Nasopharyngeal Carcinoma Staging by CT and MRI

NASOPHARYNGEAL CARCINOMA
STAGING BY COMPUTED TOMOGRAPHY AND

MAGNETIC RESONANCE IMAGING
Thesis
Submitted to the Faculty of Medicine
Alexandria University
In partial fulfillment of the requirements for the degree of
Master of Radiodiagnosis
By
Islam Mohamed El Gezeiry

MBBCh, University of Alexandria
Faculty of Medicine
Alexandria University
2014
Presented by

For the Degree of
Master of Radiodiagnosis
Examiners Committee:
Prof. Dr. Shadia Abou Seif Helmy
Approved
Professor of Radiodiagnosis
Faculty of Medicine
University of Alexandria
Prof. Dr. Mahmoud Lotfy El-Sheikh
....
Faculty of Medicine
Prof. Dr. Ahmed Abdel Khalek Abdel Razek
Faculty of Medicine
University of Mansoura
Date:
/ /
SUPERVISORS
Prof. Dr. Shadia Abou Seif Helmy
Faculty of Medicine
.
Prof. Dr. Mohamed Basiouny Atalla
Professor of Otorhinolaryngology
Faculty of Medicine
Ass. Prof. Dr. Mohamed Eid Ibrahim

Assistant Professor of Radiodiagnosis
Faculty of Medicine
ACKNOLEDGEMENT
Praise to Allah, the Most Gracious and the Most Merciful
Who Guides me to the right way
First and foremost, my thanks are directed to Professor Dr.
Shadia Abou Seif Helmy, Professor of Radiodiagnosis, Faculty of

Medicine, University of Alexandria, for her unlimited help and
continuous insistence on perfection, without her constant supervision, this
thesis could not have achieved its present form.
Many thanks and appreciation to Ass. Prof. Dr. Mohamed Eid
Ibrahim, Assistant Professor in Radiodiagnosis, Faculty of Medicine,

University of Alexandria, for his supervision and encouragement and for
his kindness throughout the work.
I am greatly indebted to Prof. Dr. Mohamed Basiouny Atalla,
Professor of Otorhinolaryngology, Faculty of Medicine, University of
Alexandria, for fruitful suggestions and wise guidance created this thesis.
Last but not the least, special thanks to my parents and my wife
for their continuous encouragement and kind support during the progress
of this work, to whom I owe a lot of things more than I can count.
CONTENTS
LIST OF ABBREVIATIONS --------------------
LIST OF TABLES----------------------------------
II
LIST OF FIGURES--------------------------------
III
INTRODUCTION-----------------------------------
AIM OF THE WORK------------------------------
34
PATIENTS AND METHODS---------------------
35
RESULTS---------------------------------------------
38
DISCUSSION----------------------------------------
69
SUMMARY------------------------------------------
84
CONCLUSION--------------------------------------
87
REFERENCES--------------------------------------
88
ARABIC SUMMARY-----------------------------
Abbreviations
ABBREVIATIONS
NPC
Nasopharyngeal Carcinoma
EBV
Epstein-Barr virus
PPS
Parapharyngeal space
PMS
Pharyngeal mucosal space
MS
Masticator space
PS
Parotid space
CS
Carotid space
BS
Buccal space
RPS
Retropharyngeal space
DS
Danger space
PVS
Perivertebral space
LRP
Lateral retropharyngeal
LN
Lymph nodes
WHO
World Health Organization
AJCC
American Joint Committee on Cancer
CN
Cranial nerve
RT
Radiotherapy
IMRT
Intensity Modulated Radiotherapy
CRT
Combined chemotherapy and radiotherapy
RPLN
Retropharyngeal lymph nodes
PPF
Pterygopalatine fossa
PNS
Perineural spread
LIST OF TABLES
Table
Page
(1)
Distribution of studied cases according to demographic

data
38
(2)
Distribution of studied cases according to side involved
38
(3)
Distribution of studied cases according to neck spaces

involved
38
(4)
Distribution of studied cases according to extension

pattern
39
(5)
Distribution of studied cases according to paranasal sinus

involvement
39
(6)
Distribution of studied cases according to pterygopalatine

fossa involvement
40
(7)
Distribution of studied cases according to skull base bone

involvement pattern
40
(8)
Distribution of studied cases according to foramina
40
(9)
Distribution of studied cases according to perineural

spread
41
(10)
Distribution of studied cases according to lymph nodal

involvement
41
(11)
Distribution of studied cases with cervical

metastases according to criteria of involvement
nodal
41
(12)
Distribution of studied cases according to primary tumor

T-stage
42
(13)
Distribution of studied cases according to lymph nodes

involvement N-stage
42
(14)
Distribution of studied cases according to TNM stage
42
ii
LIST OF FIGURES
Figure
(1)
Page
Graphic of the nasopharyngeal mucosal space seen from
behind.
(2)
A graphic of skull base from below shows spaces of
suprahyoid neck relationships to skull base with emphasis on

the pharyngeal mucosal space.
(3)
Axial graphic of the nasopharyngeal mucosal space.
(4)
Mid-line sagittal graphic of the nasopharynx.
(5)
Lateral radiograph of the nasopharynx showing enlarged
adenoids.
(6)
A graphic showing the lateral wall structures of the
nasopharynx.
(7)
Spaces related to the nasopharynx.
(8)
A graphic of the neck as seen from left anterior view showing specific
10
margins of the levels of the imaging-based classification for the lymph

nodes of the neck
(9)
A lateral radiograph of mildly enlarged adenoid.
12
(10)
The superior end of the para-pharyngeal space just before it
13
abuts the skull base.

(11)
Axial T2w image at the level of the opening of the Eustachian
15
tube.
(12)
Axial T1w image of the pharyngeal mucosal space at the
15
level of the Eustachian tube opening.

(13)
Sagittal T1w image of the pharynx.
16
(14)
Coronal enhanced fat-saturated T1 MR image.
16
(15)
Coronal enhanced fat-saturated T1w MR Image.
17
iii
Figure
(16)
Page
Axial T2w image of the nasopharynx with demonstration of
17
the related spaces.

(17)
Shaded triangular area corresponding to the supraclavicular
22
fossa used in staging carcinoma of the nasopharynx.

(18)
(Right)Axial T2wI MR shows large right NP mass.
24
(Left) Axial bone CT showing enlarged right foramen ovale.

(19)
Patient presenting with a left nasopharyngeal tumor.
25
(20)
Axial TSE T2-weighted image showing left nasopharyngeal
26
tumor extending to the pterygo-palatine fossa.

(21)
Contrast-enhanced SE T1-weighted MR images with fat
27
saturation illustrating different pathways of extension in a

patient suffering nasopharyngeal tumor.
(22)
Contrast-enhanced T1-weighted MR images in a patient
28
presenting with direct lateral extension through the

pharyngobasilar fascia to the prestyloid compartment of the
parapharyngeal space, and the infratemporal fossa, with
infiltration of the pterygoid muscles.
(23)
Spread of an advanced nasopharyngeal tumor.
29
(24)
(a) Non-enhanced T1-weighted MR image without fat
29
saturation of a nasopharyngeal tumor infiltrating the clivus

bone marrow.
(b) Enhanced T1-weighted image with fat saturation, the
tumor extends laterally to the jugular foramen and the
hypoglossal canal.
iv
Figure
(25)
Page
Patient presenting with a nasopharyngeal tumor (a) revealed
30
a serous otitis. (b) Posterior spread to the retropharyngeal

space and parapharyngeal space. (c) A left retropharyngeal
node and inferior extension to the oropharynx.
(26)
(a) CT images illustrate a nasopharyngeal tumor extending to
31
the foramen lacerum.

(b) Note the enlargement of the foramen lacerum.
(27)
(a) CT depicts small skull base erosions.

(b) MRI non-enhanced T1-weighted sequence without fat
saturation shows infiltration of sphenoid bone marrow.
31
Introduction
INTRODUCTION
Epidemiology (1)
Nasopharyngeal carcinoma (NPC) is a rare malignancy in most
parts of the world, with an incidence well under 1 per 100,000 personyears. Populations with elevated rates include the natives of Southeast
Asia, the natives of the Arctic region, and the Arabs of North Africa
and parts of the Middle East. (1)
Sex and Age Distributions:
In almost all populations, the incidence of NPC is 2- to 3- folds
higher in males than in females. (1)
In most low-risk populations, NPC incidence increases
monotonically with increasing age. In contrast, in high-risk groups, the
incidence peaks around ages 50 to 59 years and declines thereafter.
Risk factors:
1. Epstein-Barr virus:
Primary EBV infection is typically subclinical; the virus is
associated with later development of several malignancies,
including NPC.
(2)
NPC patients were found to express antibodies
against EBV. Antibody against EBV capsid antigen is now

established as the basis of a screening test for NPC in high-risk
populations. (3-8)
Introduction
2. Salt-Preserved Fish and Other Foods:

NPC risk is also elevated in association with salt preserved
fish and other preserved food items, including meats, eggs, fruits,
and vegetables (excluding type I NPC). (9)
3. Tobacco, and Other Smoke:

The majority of case-control studies examining cigarette
smoking and risk of NPC in a variety of populations reported an
increased risk of 2- to 6-fold. In one U.S. study, an estimated two
thirds of type I NPC was attributable to smoking, but risk of type II
or III NPC was not associated with smoking. (10-20)
4. Occupational Exposures:
Occupational exposure to fumes, smokes, dusts, or
chemicals overall was associated with a 2- to 6-folds higher risk of
NPC in some studies. (15, 18, 21, 22)
5. Other Exposures:
Most studies investigating prior chronic ear, nose, throat, and
lower respiratory tract conditions found that they approximately
doubled the risk of NPC. (11-13)
6. Familial Clustering:
Familial aggregation of NPC has been widely documented in
high-incidence,
intermediate-incidence,
populations. (23-39)
and
low-incidence
Introduction
ANATOMY OF THE NASOPHARYNX AND

RELATED SPACES (40-42)
The nasopharynx extends from the base of the skull to the lower
border of the soft palate. The rigid pharyngobasilar fascia keeps it from
collapsing at the back and sides. At the front the upper part communicates
with the nose through the choanae, while below this the soft palate forms
its anterior wall. The space between the lower border of the soft palate
and the posterior pharyngeal wall through which the nasopharynx joins
the oral part of the pharynx is the oropharyngeal isthmus. The soft palate
becomes a mobile floor, like a trap door, when elevated during
swallowing to meet the posterior wall, so closing the isthmus.
(43)
The nasopharynx communicates anteriorly with the posterior nasal

choanal openings and downward with the oropharynx. (Fig. 1)
Fig. 1 Graphic of the nasopharyngeal mucosal space/surface seen from behind shows
communication of the nasopharyngeal mucosal space anteriorly with the posterior
nasal choanal openings. (41)
The roof and posterior margins are formed by the sphenoid bone,
the clivus and the insertion of the prevertebral muscles into the skull base.
Introduction
Fig. 2 A graphic of skull base from below shows spaces of suprahyoid neck
relationships to skull base with emphasis on the pharyngeal mucosal space. Notice the
pharyngeal mucosal space abuts a broad area of the sphenoid and occipital bones. The
foramen lacerum, the cartilaginous floor to the anteromedial horizontal petrous
internal carotid artery canal, is within this abutment area. Malignant tumors of the
nasopharyngeal mucosal space can access the intracranial compartment via the
foramen lacerum. (41)
Fig. 3 Axial graphic of the nasopharyngeal mucosal space (in blue) shows the
superior pharyngeal constrictor and levator veli palatine muscles are within the space.
The middle layer of the deep cervical fascia provides a deep margin to the space. The
retropharyngeal space is behind and the parapharyngeal space is lateral to the
pharyngeal mucosal space. (41)
Introduction
This roof shows downward slopping and is formed, cranially-tocaudally, by the basisphenoid, the basiocciput, and the anterior aspect of
the first two cervical vertebrae. On this wall a prominence produced by a
mass of lymphoid tissue, more prominent in childhood, is known as
pharyngeal tonsils (adenoids). (40) (Fig. 4 & Fig. 5)
Fig. 4 Mid-line sagittal graphic of the nasopharynx.
Prominent adenoids
Fig. 5 Lateral radiograph of the nasopharynx showing enlarged adenoids.
(44)
Introduction
The lateral margins are made up by the pharyngeal constrictors and

the torus tubaris, in the center of which is the opening of the Eustachian
tube. (Fig. 4 & Fig. 6) The Eustachian tube enters the nasopharynx
through the sinus of Morgagni, a defect in the anterior portion of the
pharyngobasilar fascia, which is above the superior pharyngeal
constrictor muscle and along the upper posterior border of the medial
pterygoid plate. The levator veli palatini muscle also enters through the
sinus of Morgagni.
Fig. 6 A graphic showing the lateral wall structures of the nasopharynx.
(45)
Behind the ostium of the Eustachian tube is a deep recess, the

pharyngeal recess (fossa of Rosenmller). The fossa of Rosenmller is
the most common site of origin in nasopharyngeal carcinoma (NPC).
The inverted J-shape of the torus tubaris explains why the fossa of
Rosenmller appears posterior (on axial images) and superior (on coronal
images) to the Eustachian tube orifice.
Introduction
The inferior margin of the nasopharynx is the level of the hard

palate and Passavants muscle. This muscle is composed of fibers that
arise laterally from the palatopharyngeus muscle and the lateral aspect of
the posterior border of the hard palate. The fibers encircle the pharynx
inside the superior constrictor muscle.
The lateral nasopharyngeal walls are supported by the margins of
the superior constrictor muscle and the pharyngobasilar fascia.
Spaces related to the nasopharynx

In the suprahyoid neck, three layers of deep cervical fascia are
detected. These fascias are: (41)
1- Superficial layer (investing fascia)
2- Middle layer (buccopharyngeal fascia)
3- Deep layer (prevertebral fascia)
Spaces related to the nasopharynx are defined by these three layers
of deep cervical fascia. (Fig. 7)
Introduction
Fig. 7 (PPS) parapharyngeal space, (PMS) pharyngeal mucosal space, (MS)

masticator space, (PS) parotid space, (CS) carotid space, (BS) buccal space, (RPS)
retropharyngeal space, (DS) danger space, (PVS) perivertebral space.
1. Parapharyngeal space
(41)
(41)
A slit-like space lateral to the nasopharynx extending down from

the base of the skull. Potential space filled with loose connective tissue.
The space is pyramidal in shape with apex directed towards the lesser
cornu of the hyoid bone and the base towards the skull base. It extends
from skull base to mid-oropharynx. It is lined medially by the superior
constrictor muscles of the pharynx, tensor and levator veli palatini
muscles. Laterally is lined by the mandible, the deep part of the parotid
gland, and medial pterygoid muscle. Anteriorly lying is the buccinator
muscle, the pterygoid, and the mandible. Posteriorly is the carotid sheath.
The parapharyngeal space contains fat, ascending pharyngeal and internal
maxillary arteries, pharyngeal venous plexus, and branches of the
mandibular nerve.
Introduction
2. Retropharyngeal space and the prevertebral spaces (41)

Lie between the nasopharynx and the vertebral bodies. The
retropharyngeal space extends as a potential space from the skull base to
about the level of T4 vertebral body and it serves as a conduit through
which infections spread from the neck to the mediastinum. It contains fat
and lymph nodes (lateral nodes of Rouvier and medial nodes).
3. Nasopharyngeal masticator space (41)

Lies lateral to the nasopharynx behind the posterior wall of the
maxilla and extends from the base of the skull to the hyoid bone. It
contains medial and lateral pterygoid muscles. No fascia defines this
space which was previously named as infratemporal fossa. This term was
used to describe the area between the pterygopalatine fossa and
zygomatic arch. Medial to this, the roof is formed by the inferior surface
of the middle cranial fossa and is pierced by the foramen ovale and
foramen spinosum.
Lymphatic drainage of the nasopharynx

Lymphatic drainage is abundant in the nasopharynx, as evidenced
by the high rate of nodal metastases found by the time of diagnosis of
nasopharyngeal carcinomas. Three main groups of submucosal collecting
pathways drain the pharynx, the superior, the middle, and the inferior
pathways. The superior pathway drains the oropharynx, soft palate,
Eustachian tube, fossa of Rosenmller, tympanic cavity, and nasal fossae.
(45)
Introduction
Fig. 8 A graphic of the neck as seen from left anterior view. Drawing shows specific
margins of the levels of the imaging-based classification for the lymph nodes of the
neck. Note that the line of separation between levels I and II is the posterior margin of
the submandibular gland. Separation between levels II and III and level V is the
posterior edge of the sternocleidomastoid muscle. The line of separation between
levels IV and V is the oblique line extending from the posterior edge of the
sternocleidomastoid muscle to the posterior edge of the anterior scalene muscle.
Posterior edge of internal jugular vein separates level IIA and IIB nodes. Carotid
arteries separate levels III and IV from level VI. Top of manubrium separates levels
VI and VII. (46, 47)
Within the retropharyngeal space there are lateral retropharyngeal

(LRP) lymph nodes of Rouvire. These nodes are the first nodes in the
lymphatic drainage of the nasopharynx and maybe identified as discrete
3-5 mm nodules. (48)
10
Introduction
The adenoids, or pharyngeal tonsils, are lymphatic tissue located in

the midline roof of the nasopharynx. Prominent adenoids are typically
present in children, and of such adenoids are not identified, the patient is
either in an immune deficiency state or has immune deficiency syndrome.
The maximal size of the adenoids occurs at about 5 years of age, around
the time of puberty, gradual adenoidal involution normally begins. The
majority of individuals have lost most this adenoidal tissues by 30 years
of age. (49-51)
11
Introduction
RADIOLOGICAL ANATOMY OF THE

NASOPHARYNX (41, 52)
Plain X-ray film (48)
Fig. 9 A lateral radiograph of mildly enlarged adenoid. (48)
Conventional radiographs are used to evaluate patients with stridor,

suspected retropharyngeal abscess or adenoid hypertrophy.
Lateral soft tissue neck radiography may be helpful in making the
diagnosis of nasopharyngeal masses. Perform the study during inspiration
with neck held in normal extension. (53)
The posterior wall of the pharynx forms a soft-tissue shadow
curving posteroinferiorly below the body of the sphenoid and anterior to
the cervical vertebrae. This shadow thins as it passes down anterior to the
upper cervical vertebrae, measuring 3mm anterior to C4. Below this the
wall is thicker but should not exceed the AP diameter of the cervical
12
Introduction
vertebrae. In children, lymphoid tissue results in a relatively thicker

posterior wall, measuring up to 5 mm anterior to C4 and up to 12 mm
anterior to C6 (Fig. 9).
(48)
Widening of the soft tissues observed between the radiolucent

airway and the spine is pathologic until otherwise proven.
CT anatomy of the nasopharynx (41)

Axial contrast enhanced CT (CECT) of the nasopharynx:
Fig. 10 The superior end of the parapharyngeal space just before it abuts the skull
base, Notice the 4 major spaces surrounding the parapharyngeal space, the pharyngeal
mucosal, masticator, parotid and carotid spaces. (41)
CT evaluation of the nasopharynx is achieved with axial images

with the patient lying supine. The head should be aligned carefully with
the cranio-caudal axis, usually with the hard palate perpendicular to the
table top and a scan plane parallel to the inferior orbital meatal plane.
Poor positioning may result in an appearance that either simulates
pathology or occasionally make pathology difficult to see. (54)
13
Introduction
At CT the tissue density of the fascia itself is inseparable from that

of the adjacent musculature. The normal fat content of surrounding
spaces compounded by associated muscle atrophy in the elderly patients
will produce low density regions permitting a CT identification of the
fascial planes. (48)
The fat content of the paranasopharyngeal space allows one to
easily identify it as a low density tissue plane lying between the pterygoid
and pharyngeal musculature. Inferiorly the buccopharyngeal fascia is
continuous with the covering of the nasopharynx and esophagus. The
infratemporal fossa lies lateral to the paranasopharyngeal space. The
infratemporal fossa is bounded laterally by the zygomatic arch. Within
this space is most of the mandible, pterygoid, masseter, and parts of the
temporalis muscle and deep lobe of the parotid gland. (42, 55)
Other spaces defined by these fascial planes are important because
their contents determine the cell of origin of some tumors. A potential
space, the retropharyngeal space, exists between the pharyngobasilar
fascia and the prevertebral fascia. This space contains the chains of lymph
nodes lying to either side of the midline posteriorly. (42)
Laterally the carotid sheath forms a posterolateral boundary to the
retropharyngeal space. Within the carotid sheath lie the carotid vessels,
sympathetic chains, and the vagus and proximal parts of XI and XII
cranial nerves together with major deep lymphatic chains intimately
associated with the jugular vein. (42)
14
Introduction
Normal MRI anatomy of the nasopharynx (41)

The routine MR examination after obtaining scout images, sagittal,
axial and coronal T1-weighted images, and axial T2-weighted images,
with post-contrast (gadolinium-DTPA) injection T1-weighted images are
obtained. Comparison of the pre- and post-contrast images is made to
determine the areas of enhancement and to differentiate these areas from
fat.
Axial T2w Image of the nasopharyngeal mucosal space: (41)
Fig. 11 Axial T2w image at the level of the opening of the Eustachian tube
Axial T1w image of the nasopharyngeal mucosal space: (49)
Fig. 12 Axial T1w image of the pharyngeal mucosal space at the level of the
Eustachian tube opening.
15
Introduction
Sagittal T1w image of the pharynx:

Fig. 13 Sagittal T1w image of the pharynx (48)
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Soft palate
Adenoids
Middle turbinate
Inferior turbinate
Hard palate
Intrinsic muscle of
tongue
Genioglossus
Mandible
Myelohyoid muscle
Hyoid bone
Epiglottis
Vocal cord
Thyroid cartilage
Nasopharynx
Oropharynx
Corniculate cartilage
Arytenoid cartilage
Cricoid cartilage
Coronal T1w images of the nasopharynx: (41)
Fig. 14 Coronal enhanced fat-saturated T1 MR image shows the pharyngeal mucosal

space surface enhances.
16
Introduction
Fig. 15 Coronal enhanced fat-saturated T1w MR image reveals the enhancing sheet of
mucosa with the torus tubarius (cartilaginous Eustachian tube) and lateral pharyngeal
recess.
Fig. 16 Axial T2w image of the nasopharynx with demonstration of the related
spaces. (41)
The superficial nasopharyngeal landmarks and deep fascial planes

of the nasopharynx are normally bilaterally symmetrical. The most
prominent of these is the torus tubaris, the cartilaginous part of the
Eustachian tube, usually seen on MR as a medium- to high-intensity
protuberance projecting into the aerated nasopharyngeal cavity. (42)
17
Introduction
In the mid- to upper nasopharynx, the tensor veli palatini and

levator veli palatini muscle bundles are routinely shown by MR as they
descend from their origin at the base of the skull to their insertion in the
soft palate. At the transition from the nasopharynx to the oropharynx, the
soft palate, tensor and levator palate, and pharyngeal constrictor muscles
blend together, producing a low-intensity signal which surrounds the
airway. (42)
Although the tonsils may normally be quite large, they should not
cause a mass effect involving the airway or deep soft tissue planes. A Ushaped ring of high-intensity tissue near the base of the tongue,
corresponding to the lingual tonsil, is also routinely demonstrated on long
TR sequences. (56)
Below the nasopharyngeal mucosa and pharyngobasilar fascia,
symmetrical fatty parapharyngeal spaces extend bilaterally from the base
of the skull to the oropharynx. (42)
18
Introduction
PATHOLOGY OF THE NASOPHARYNGEAL

CARCINOMA
Normal histology of the nasopharynx
The anterior and cranial portions of the nasopharynx are lined by
respiratory mucosa with ciliated columnar epithelium with goblet cells
and foci of metaplastic squamous epithelium. Squamous mucosa
predominates in the lower nasopharynx adjacent to the oropharynx. Small
seromucinous glands and aggregates of lymphoid tissue are present in the
submucosa throughout the nasopharynx as a normal finding without
qualifying as chronic inflammation. (57)
Pathology of nasopharyngeal carcinoma (NPC)

Three subtypes of NPC are recognized in the World Health Organization
(WHO) classification 2005: (58-60)
1. Keratinizing squamous cell carcinoma (type I)
2. Non-keratinizing carcinoma:
a) undifferentiated (type II)
b) differentiated (type III)
3. Basaloid squamous cell carcinoma
Most cases in childhood and adolescence are type III, with a few
type II cases. Type II and III are associated with elevated Epstein-Barr
virus titers, but type I is not. Types II and III may be accompanied by an
inflammatory infiltrate of lymphocytes, plasma cells, and eosinophils,
which are abundant, giving rise to the term lymphoepithelioma.
19
(61, 62)
Introduction
Staging
The tumor, node, metastasis (TNM) classification of the American
Joint Committee on Cancer is usually used to determine the tumor staging
This latest TNM classification (AJCC 7th ed.) takes into account Hos
modifications for NPC which utilizes the prognostic importance of
affected nodes extending into the lower cervical and supraclavicular
areas. (63)
Definition of TNM
Primary Tumor (T)
TX
T0
Tis
T1
Primary tumor cannot be assessed

No evidence of primary tumor
Carcinoma in situ
Tumor confined to the nasopharynx, or tumor extends to oropharynx
and/or nasal cavity without parapharyngeal extension*
T2 Tumor with parapharyngeal extension*
T3 Tumor involves bony structures of skull base and/or paranasal
sinuses
T4 Tumor with intracranial extension and/or involvement of cranial
nerves, hypopharynx, orbit, or with extension to the infratemporal
fossa/masticator space
*Note: Parapharyngeal extension denotes posterolateral infiltration of tumor.
20
Introduction
Regional Lymph Nodes (N)

The distribution and the prognostic impact of regional lymph nodes
spread from nasopharynx cancer, particularly of the undifferentiated type,
are different from those of other head and neck mucosal cancers and
justify the use of a different N classification scheme.
Regional lymph nodes cannot be assessed
No regional lymph node metastasis
Unilateral metastasis in cervical lymph node(s), 6 cm or less
in greatest dimension, above the supraclavicular fossa,
and/or unilateral or bilateral, retropharyngeal lymph nodes,
6 cm or less, in greatest dimension*
Bilateral metastasis in cervical lymph node(s), 6 cm or less
N2
in greatest dimension, above the supraclavicular fossa*
Metastasis in a lymph node(s)* >6 cm and/or to
N3
supraclavicular fossa*
N3a Greater than 6 cm in dimension
N3b Extension to the supraclavicular fossa**
*Note: Midline nodes are considered ipsilateral nodes.
NX
N0
N1
**Note: Supraclavicular zone or fossa is relevant to the staging of

nasopharyngeal carcinoma and is the triangular region originally
described by Ho. It is defined by three points (Fig. 17):
1. The superior margin of the sternal end of the clavicle.
2. The superior margin of the lateral end of the clavicle.
3. The point where the neck meets the shoulder.
Note that this would include caudal portions of levels IV and VB. All
cases with lymph nodes (whole or part) in the fossa are considered N3b.
21
Introduction
Fig. 17 Shaded triangular area corresponding to the supraclavicular fossa used in

staging carcinoma of the nasopharynx. (64)
Distant Metastasis (M)
M0
No distant metastasis
M1
Distant metastasis
Stage grouping
Stage 0
Stage I
Stage II
Stage III
Stage IVA
Stage IVB
Stage IVC
Tis
N0
M0
T1
N0
M0
T1
T2
T2
T1
T2
T3
T3
T3
T4
T4
T4
Any T
N1
N0
N1
N2
N2
N0
N1
N2
N0
N1
N2
N3
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
M0
Any T
Any N
M1
22
Introduction
Presentation (41)
Early stage NPC is difficult to diagnose clinically because of its
hidden localization in the nasopharynx, and most patients present with
advanced stage of the disease.
Asymmetric neck swelling due to lymphadenopathy.
Nasal symptoms: Epistaxis, bloody, rhinorhea, nasal
obstruction.
Ear symptoms: infection (Recurrent otitis media), deafness,
and tinnitus.
Ophthalmic symptoms: Diplopia, visual loss, squint, Ptosis.
Headache.
Blood in saliva.
Facial numbness.
Cranial nerve palsies; CN 9-12.
23
Introduction
IMAGING OF THE NASOPHARYNGEAL

CARCINOMA
Fig. 18 (Right) Axial T2w MR image shows large right NP mass, extending into
pterygoid muscle (arrow), & posterior to surround ICA (open arrow). Mastoid fluid
(curved arrow) due to Eustachian tube obstruction. ( Left) Axial bone CT image
showing enlarged right foramen ovale (arrow) from perineural V3 NPC spread with
adjacent skull base destruction (open arrows). (Curved arrow) normal foramen ovale.
(41)
Aggressive mass centered in lateral pharyngeal recess of the

nasopharynx (fossa of Rosenmller) with deep extension and cervical
adenopathy. It arises from the lateral nasopharynx + posterolateral nasal
cavity. It is usually several centimeters when diagnosed. (41)
Morphology:
Poorly marginated nasopharyngeal mucosal space mass with deep
extension and invasion. (41)
24
Introduction
Extension patterns of the nasopharyngeal carcinoma: (65, 66)

As explained, nasopharyngeal tumors spread along well-defined routes.
1. Anterior spread
Nasopharyngeal tumors often spread to the nasal fossa, which is
not separated from the nasopharynx by any anatomic barrier (Fig. 19).
From the nasal fossa, the tumor may easily infiltrate the pterygopalatine
fossa through the sphenopalatine foramen (Fig. 20). The earliest sign of
involvement of the pterygopalatine fossa is replacement of its normal fat
content by tumoral tissue (Fig. 21). (66)
Fig. 19 Patient presenting with a left nasopharyngeal tumor (anterior arrow), showing
intermediate signal intensity on T2-weighted MR image. Note the anterior extension
to the left choana (arrowhead). Associated serous otitis (posterior arrow).
25
(66)
Introduction
Fig. 20 Axial TSE T2-weighted image showing left nasopharyngeal tumor extending
to the pterygopalatine fossa (arrow) (66)
Once tumor gains access to the pterygopalatine fossa, it can spread

into (Fig. 21): (66)
o The foramen rotundum along the maxillary nerve (V2)
o The inferior orbital fissure and further the orbital apex, from where
the tumor can extend intracranially through the superior orbital
fissure.
o The infratemporal fossa, where the masticator muscles are at risk
of invasion. Erosion of the pterygoid process may occur. Perineural
extension along the mandibular nerve (V3) into the foramen ovale
and the endocranium is also possible (Fig. 22)
o The vidian canal along the pterygoidien nerve and further to the
petrous apex.
26
Introduction
Fig. 21 Contrast-enhanced SE T1-weighted MR images with fat saturation illustrating

different pathways of extension in a patient suffering nasopharyngeal tumor. (a)
Extension through the sinus of Morgagni, weakest point of the pharyngobasilar fascia
(arrow). (b) Extension into the pterygopalatine fossa (arrow), neural crossroad within
the skull base. (c) From the pterygopalatine fossa, the tumor extends to the inferior
orbital fissure (arrow). (d) Extension to the infratemporal fossa (arrow) and to the
pterygoid canal with perineural spread along the vidian nerve (arrowhead). (e)
Perineural spread along the mandibular nerve (V3) extending to the foramen ovale
(arrow) and the cavernous sinus (arrowhead) (66)
27
Introduction
2. Lateral spread
Lateral extension to the parapharyngeal spaces can occur directly
through the pharyngobasilar fascia (Fig. 22), or indirectly through the
sinus of Morgagni, the fascias point of weakness. Further lateral spread
involves the infratemporal fossa and the masticator space infiltrating the
pterygoid muscles. From the masticator space, perineural extension along
the mandibular nerve (V3) may occur, leading to infiltration of the
foramen ovale and the cavernous sinus (Fig. 23). (66)
Fig. 22 Contrast-enhanced T1-weighted MR images in a patient presenting with direct

lateral extension through the pharyngobasilar fascia to the prestyloid compartment of
the parapharyngeal space (a, arrow), and the infratemporal fossa, with infiltration of
the pterygoid muscles (b, arrow) (66)
3. Posterior spread
Nasopharyngeal
tumors
can
extend
posteriorly
to
the
retropharyngeal space and the prevertebral muscles (Fig. 23). Destruction

of vertebral bodies is occasionally seen in very advanced tumors.
Posterolateral extension may involve the jugular foramen and the
hypoglossal canal (Fig. 24), with possible but rare spread to the posterior
fossa. This posterior extension may result in hypoglossal nerve (XII)
palsy. (66)
28
Introduction
Fig. 23 Spread of an advanced nasopharyngeal tumor. (a) Posterior extension to the

retropharyngeal space and prevertebral muscles (arrow). (b) Lateral extension to the
retrostyloid compartment of the parapharyngeal space, with encasement and
narrowing of the internal carotid artery (arrow). (c) Extension to the infratemporal
fossa (arrow) with intracranial spread into the cavernous sinus through the foramen
ovale (arrowhead). (66)
Fig. 24 Non-enhanced T1-weighted MR image of a nasopharyngeal tumor extending

posteriorly, infiltrating the clivus bone marrow (a, arrowhead), well identified on this
sequence by signal loss within the normally hyperintense bone marrow. (b) On the
enhanced T1-weighted fat saturation image, the tumor is seen to extend laterally to the
jugular foramen (anterior arrow) and the hypoglossal canal (XII) (posterior arrow). (66)
29
Introduction
4. Inferior spread
Some nasopharyngeal tumors present with submucosal spread into
the oropharynx, involving the tonsillar fossa (Fig. 24). This extension
may take place submucosally and thus escape detection by endoscopy,
although not detection by imaging. (66)
Fig. 25 Patient presenting with a nasopharyngeal tumor, clinically revealed by a

serous otitis (a, arrowhead) without lateral extension but a posterior spread to the
retropharyngeal space (arrow) and posterior parapharyngeal space (b, arrow). (c) A
left retropharyngeal node (arrow). Note the inferior extension to the oropharynx
(arrowhead). (66)
5. Superior spread
Nasopharyngeal tumor can spread through the foramen lacerum,
even if it is contained by the pharyngobasilar fascia. If the tumor extends
to the tough fibrous cartilage which closes the foramen lacerum,
intracranial extension may occur (Fig. 26).
Superior spread with erosion of the clivus and the sphenoid sinus is
also possible leading to intracranial extension (Fig. 27). (66)
30
Introduction
Fig. 26 (a) Coronal reconstruction of contrast enhanced CT image illustrating a

nasopharyngeal tumor extending to the foramen lacerum. (b) Coronal bone window
CT image. Note the enlargement of the foramen lacerum. (66)
Fig. 27 Patient presenting with a nasopharyngeal tumor showing direct superior

extension and infiltration of the sphenoid bone. (a) CT depicts small skull base clival
erosions, (b) whereas MRI, in particular the non-enhanced T1-weighted sequence
without fat saturation, shows a much more important infiltration of sphenoid bone
marrow. (66)
Intracranial extension of nasopharyngeal tumors is possible via

different pathways such as the foramen lacerum, the foramen ovale and
erosion of the skull base. Many studies have illustrated the good
sensitivity of MRI to detect such extension, which is usually perineural.
The frequency of intracranial abnormalities on MRI is 30%.
(67)
Nasopharyngeal tumors with intracranial extension are classified as T4

tumors according to the TNM staging system.
(67, 68)
Intracranial spread is
usually extra-axial, resulting in involvement of the cavernous and

temporal meninges. (66)
31
Introduction
Staging and Treatment: (69)

Taking into account the various TNM features, NPC patients are
then staged accordingly from Stage 0 to Stage IV. Several features of
note are:
a) T3 disease indicates a patient is at least Stage III
b) T4 disease places the patient at Stage IV
c) N3 disease (i.e. single node >6 cm in size; supraclavicular
nodes) indicates a patient is at least Stage IVb
d) M1 disease places the patient at stage IVc.
Correct staging enables the clinician to determine which treatment
modality is best for the patient. A detailed discussion of the treatment
options is beyond the scope of this paper. In brief, radiotherapy (RT) is
the mainstay of treatment for NPC, as the differentiated and
undifferentiated non-keratinizing squamous cell carcinomas (formerly
named type II and III) are very radiosensitive.
(70, 71)
Conventional
external beam RT was the traditional method of treatment. However, the

tumor could not be maximally irradiated without damaging adjacent
structures such as the parotid glands. With the advent of conformal
techniques, and in particular, intensity-modulated radiotherapy(IMRT),
doses of up to 70 Grays may be delivered with relative sparing of the
adjacent soft tissues. Limitations still remain with very large tumors, for
example, T4 tumors, where NPC may be so close to vital structures such
as the optic chiasm that the latter cannot be spared if the full RT dose
were to be administered.
Combined
chemotherapy
using
platinum-based
drugs
and
radiotherapy (CRT) is given for patients with T3 disease and nodal
32
Introduction
disease >N1. Patients with T4 and N3 disease may receive neoadjuvant

chemotherapy with platinum-based combination chemotherapy followed
by definitive RT with concurrent chemotherapy.
(71)
Patients with T1/T2
N1 disease are also treated with CRT although this is a controversial topic
and beyond the scope of this article.
33
Aim of the work
AIM OF THE WORK

The aim of this work is to describe the role of state of the art cross
sectional imaging computed tomography and magnetic resonance
imaging (CT & MRI) in the staging of nasopharyngeal carcinoma.
34
Patients and methods
PATIENTS AND METHODS

This study included 20 patients presenting with pathologically
proven nasopharyngeal carcinoma referred to the Radiodiagnosis
Department at the Alexandria Main University Hospital.
All the studied patients were subjected to the following:

1. Complete history taking.
2. Thorough clinical ENT examination.
3. The medical ethics were considered. The patient was aware of the
examination, patient's approval was obtained.
4. Multi-detector Computed Tomography examination especially bone
algorithm as well as post contrast sequences.
Patients lying supine were instructed to take shallow breaths and
refrain from swallowing during scanning. MDCT was performed on a 16MDCT scanner (Philips MX16, Philips Healthcare) with tube voltage,
120 kV; effective tube current, 150 mAs; collimation, 0.75 mm; table
feed, 12 mm/rotation; and rotation time, 0.5 second. The effective
radiation dose for a typical scanning range of 250 mm was 3.6 mSv for
men and 4.1 mSv for women. A non-ionic contrast agent ULTRAVIST,
Bayer (each ml of injection contains 769 mg iopromide, equivalent to 370
mg iodine) was injected at a flow rate of 1 ml/sec. for 50 seconds then a
waiting time for 50 seconds then inject 50 ml at 2.5 ml/sec. and start scan
at the end of injection. The scanning range started from top of the frontal
sinus base to the tracheal bifurcation. Data set was reconstructed using a
standard soft-tissue (B 40) convolution kernel with a slice thickness of 1
mm (0.7-mm reconstruction increment). For the assessment of bone and
35
cartilage, additional data set was reconstructed using a sharp (bone)

convolution kernel (B 70).
5. MRI examination:
a. Axial: T1, T2 and T2 Fat Saturation images.
b. Coronal: T1 and T2 Fat Saturation images.
c. Sagittal: T2w images.
d. Post-Contrast T1w Fat Saturation images in 3 planes.
MR imaging was performed with a 1.5 Tesla whole-body MR imaging
system (Philips Achieva 1.5T, the Netherlands), by using a 4-channel
phased array head and neck coil. The following parameters were used:
Pre-contrast axial and coronal T1-images were obtained with SE
450/15, 90, 2 excitations, a 22-cm field of view (FOV), a 256 256
matrix, a 3-mm-thick section and a 0.9-mm gap.
Axial and sagittal T2-images were obtained with SE 4500/88, 180,
3 excitations, a 22-cm field of view (FOV), a 256 256 matrix, a 3mm-thick section and a 0.9-mm gap.
Axial and coronal fat-suppressed T2-weighted sequence obtained
with SE 2500 ms/100 ms; echo-train length, 15; 22-cm field of
view (FOV), a 256 256 matrix, 4-mm-thick section, with no
intersection gap; and 256 256 matrix size.
Post-contrast medium (Dotarem ,Guerbet (0.1 mmol/kg)) Axial,
coronal, and sagittal T1w scan with fat suppression images were
obtained with SE 500/22 ms, 2 excitations, a 22-cm field of view
(FOV), a 256 256 matrix, 3-mm section thickness and 0.5-mm
gap.
36
6. Endoscopic examination and biopsy from the suspected area with

routine histopathologic examination.
7. Correlation with pathological data.
37
Results
RESULTS
Table (1): Distribution of studied cases according to demographic
data (n=20)
Age (years)
20 >30
30 >40
40 >50
50 >60
60 >70
Sex
Male
Female
No.
3(15%)
3(15%)
6(30%)
3(15%)
5(25%)
15.0
15.0
30.0
15.0
25.0
12(60%)
8(40%)
60.0
40.0
Table (2): Distribution of studied cases according to side (n=20)
Side
Right
Left
Diffuse
No.
8(40%)
11(55%)
1(5%)
40.0
55.0
5.0
Table (3): Distribution of studied cases according to neck spaces

involvement (n=20)
No.
Space
Retropharyngeal space (RPLN)
Carotid sheath
Masticator space
38
CT
MRI
4(20%)
1(5%)
7(35%)
3(15%)
8(40%)
1(5%)
8(40%)
3(15%)
40.0
5.0
40.0
15.0
Results
Table (4): Distribution of studied cases according to extension

pattern (n=20)
No.
Extension
Anteriorly
Nasal choana
Inferiorly
Oropharynx
Superiorly
Intracranial extension
Perineural spread
Posteriorly
Retropharyngeal space (RPLN)
Posterolaterally
Carotid sheath
Laterally
Masticator space
CT
MRI
8(40%)
8(40%)
40.0
5(25%)
7(35%)
35.0
7(35%)
6(30%)
8(40%)
10(50%)
40.0
50.0
4(20%)
8(40%)
30.0
1(5%)
1(5%)
5.0
7(35%)
3(15%)
8(40%)
3(15%)
40.0
15.0
Table (5): Distribution of studied cases according to paranasal

sinuses involvement (n=20)
No. of cases
Paranasal sinus involvement
Sphenoid sinus
Maxillary antrum
39
CT
4
4(20%)
MRI
6
6(30%)
30.0
30.0
1(5%)
1(5%)
5.0
Results
Table (6): Distribution

of
studied
cases
according
pterygopalatine fossa involvement (n=20)
No.
CT
7(35%)
2(10%)
5(25%)
Pterygopalatine fossa
Right
Left
MRI
9(45%)
3(15%)
6(30%)
to
%
45.0
15.0
30.0
Table (7): Distribution of studied cases according to skull base bone

involvement pattern (n=20)
No. of cases
Bone
Lytic
Sclerotic
Mixed sclerosis and erosion
CT
18
7(40%)
5(25%)
6(30%)
MRI
17
8(40%)
3(15%)
6(30%)
40.0
25.0
30.0
Table (8): Distribution of studied cases according to neural

foraminal involvement (n=20)
No.
17(85%)
8(40%)
9(45%)
1(5%)
1(5%)
1(5%)
Foramina
Ovale
Lacerum
Jugular
Sphenopalatine
Rotundum
40
%
85.0
40.0
45.0
5.0
5.0
5.0
Results
Table (9): Distribution of studied cases according to perineural

spread (n=20)
No.
CT
8(40%)
MRI
11(55%)
50.0
Along V3
5(25%)
6(30%)
30.0
Along V2
2(10%)
3(15%)
15.0
Along vidian nerve
3(5%)
4(5%)
20.0
Facial nerve(VII)
0(0%)
1(5%)
5.0
Perineural spread
Table (10): Distribution of studied cases according to lymph nodal

involvement (n=20)
No.
Supraclavicular lymph nodes
CT
5(25%)
MRI
5(25%)
25.0
Retropharyngeal lymph nodes (RPLN)
4(20%)
8(40%)
60.0
Cervical lymph nodes

Parotid LN
14(70%)
3(15%)
14(70%)
3(15%)
70.0
15.0
Table (11): Distribution of studied cases with cervical lymph nodal

metastases according to criteria of involvement (n=20)
No.
Size enlargement
Necrosis
Extra-capsular extension
CT
16
5
3
41
%
MRI
16
5
3
80.0
25.0
15.0
Results
Table (12): Distribution of studied cases according to primary tumor

T-stage (n=20)
Primary tumor
T1
T2
T3
T4
No.
0(0%)
0(0%)
5(25%)
15(75%)
0.0
0.0
25.0
75.0
Table (13): Distribution of studied cases according to lymph nodes

involvement N-stage (n=0)
Lymph nodes
N0
N1
N2
N3a
N3b
No.
4(20%)
8(40%)
3(15%)
0(0%)
5(25%)
20.0
40.0
15.0
0.0
25.0
Table (14): Distribution of studied cases according to TNM stage

(n=20)
TNM Stage
I
II
III
IVa
IVb
IVc
No.
0(0%)
0(0%)
3(15%)
11(55%)
3(15%)
3(15%)
0.0
0.0
15.0
55.0
15.0
15.0
42
Results
Case 1:
(A)
(B)
(C)
(D)
43
Results
(E)
(F)
(G)
(H)
44
Results
Fig. 28 Case 1: 28 years old male patient with right side

nasopharyngeal carcinoma.
(A and B) Axial T2w and T2w fat suppression images: A right

nasopharyngeal
iso-intense
heterogeneous
mass
(white
arrow)
obliterating the parapharyngeal space fat and the levator veli palatini
muscle, and crossing the midline along the posterior pharyngeal wall.
(C and D) Pre- and post-contrast axial T1w images: The mass

lesion fills anteriorly the scaphoid fossa (white block arrow) of the
pterygoid process. Moderate post-contrast enhancement of the mass is
noted (D image).
(E and F) Axial CT bone window and MR T1w post-contrast

images: In the (E) image (orange curved arrow) represents the tumor
entering through the sphenopalatine foramen into the pterygopalatine
fossa (red arrow head), and hence reaching into the vidian canal (black
arrow). In the (F image) the moderately enhancing tumor filling the
pterygopalatine fossa (red arrow head) and reaching the vidian canal
(black arrow).
(G and H) Pre- and post-contrast sagittal T1w images: The lesion

extends anteriorly to the ipsilateral choana, and inferiorly reaches the
junction of the naso- and oro-pharynx (yellow arrow).
45
Results
Case 2:
(A)
(B)
(C)
(D)
46
Results
(E)
Fig. 29 Case 2: 50 years old female patient with left sided

(A) Axial CT bone window image: showing lytic lesion eroding the
clivus (red arrow) and bony borders of the vidian canal (black arrow) and
foramen rotundum (white arrow).
(B) Axial T2w image: showing intermediate signal mass lesion with
extension to the left sphenoidal sinus which showed retained secretions
(blue star), near total encasement of the petrous segment of the internal
carotid artery (yellow arrow).
(C) Axial T1w image: showing a nasopharyngeal carcinoma of the

pterygopalatine fossa invasion (green arrow).
47
Results
(D) Post-contrast sagittal T1w fat saturation image: showing

posterior invasion of the clivus with intracranial extension effacing the
pre-pontine cistern (blue arrow).
(E) Enhanced coronal
T1w fat saturation image:
The
nasopharyngeal mass reaches the cavernous sinus through the vidian

canal and the foramen rotundum (vidian and maxillary (V2) nerves
Perineural spread) with encasement of the internal carotid artery (red
arrow head) and enhancement of the maxillary nerve (yellow arrow
head).
48
Results
Case 3:
(A)
(B)
(C)
(D)
49
Results
(E)
Fig. 30 Case 3: a 30 years old female patient with left sided

(A) Axial CT bone window image: It shows widening of the petroclival fissure (black arrow) and the foramen lacerum (white arrow).
(B) Axial T1w image: a mucosal based mass lesion obliterating the left
fossa of Rosenmller showing T1 intermediate signal.
(C) Post-contrast axial 3D GRE T1w image: The moderately

enhancing tumor reaches along the lateral wall of the nasopharynx to the
pterygopalatine fossa (red arrow head) then along the vidian canal
representing perineural spread along the vidian nerve (red arrow).
(D) Post-contrast axial T1w fat saturation image: (yellow arrow)

Left sided level II enlarged metastatic lymph node with foci of necrosis
showing post-contrast enhancement.
50
Results
(E) Post-contrast sagittal T1w fat saturation image: Superior

extension of the tumor to the floor of the sphenoid sinus with minimal
intra-sinus extension (green arrow).
51
Results
Case 4:
(A)
(B)
(C)
(D)
52
Results
(E)
Fig. 31 Case 4: a 40 years old male patient with left sided

(A) Axial T1w image: A mass lesion is noted growing and expanding
the left lateral nasopharyngeal recess (Fossa of Rosenmller), showing
intermediate to low T1 signal (white arrow).
(B) Axial 3D GRE T1w image: The nasopharyngeal carcinoma grows

anteriorly to reach the pterygopalatine fossa (yellow arrow) and laterally
to reach the widened foramen ovale (red arrow) and grows along the
mandibular division of the trigeminal nerve V3 (perineural spread) in the
foramen ovale to reach intracranial cavity.
(C and D) Axial T2w and post-contrast T1w fat saturation

images: demonstrates the intracranial extra-axial left temporal
component of the nasopharyngeal carcinoma (blue arrow). Involvement
53
Results
of the cavernous sinus with total encasement of the still patent internal
carotid artery (black arrow).
(E) Post-contrast coronal T1w fat saturation image: The

nasopharyngeal lesion (white arrow) extends superiorly through the
widened foramen ovale (orange arrow) into the intracranial extra-axial
temporal mass lesion (green arrow).
54
Results
Case 5:
(A)
(B)
(C)
(D)
55
Results
(E)
Fig. 32 Case 5: a 48 years old male patient with left sided

(A) Sagittal reconstruction bone window CT image: Sclerosis and

infiltration of the bone marrow of the clivus (black arrow).
(B) Axial T1w image: Perineural spread along the mandibular division
of the left trigeminal nerve (V3), through the foramen ovale (yellow
arrow) and infiltration of the clival bone marrow (black arrow).
(C) Axial T2w image: An intracranial extra-axial temporal component

(green arrow), reaching the cavernous sinus encasing the patent internal
carotid artery siphon (blue arrow).
(D) Post-contrast coronal T1w fat saturation image: Shows the

nasopharyngeal lesion with perineural spread along the V3 division of the
mandibular nerve through the foramen ovale (yellow arrow) widening the
56
Results
foramen and extending superiorly to an extra-axial temporal mass (green

arrow) reaching the region of the trigeminal ganglion.
(E) Post-contrast sagittal T1w image: shows infiltration of the clival

bone marrow with post-contrast enhancement (black arrow).
57
Results
Case 6:
(A)
(B)
(C)
(D)
58
Results
Fig. 33 Case 6: a 65 years old male patient with right side

(A and B) Axial T2w and post-contrast T1w fat saturation

images: A right-sided nasopharyngeal carcinoma (black arrow) with
anterior extension to the pterygoid plates and scaphoid fossa (yellow
arrow).
(C) Axial Diffusion weighted image: Restricted diffusion of right

nasopharyngeal mass (white arrow)
(D) Axial T2w image: bilateral jugular chain lymph nodes (red arrows)
with necrosis in the left one.
59
Results
Case 7:
(A)
(B)
(C)
(D)
60
Results
(E)
(F)
Fig. 34 Case 7: a 38 years old male patient with diffuse bilateral

(A) Sagittal reconstruction CT bone window image: shows full

thickness moth eaten erosion of the clivus (white arrows).
(B) Contrast-enhanced axial CT image: shows a nasopharyngeal

heterogeneously
enhancing
mass
lesion
obliterating
fossae
of
Rosenmller bilaterally and filling the nasopharyngeal cavity (red

arrows).
(C) Axial T2w image: shows anterior extension of the hyperintense

nasopharyngeal lesion through both choanae into nasal cavities (orange
arrows)
(D and E) Axial T2w and Diffusion weighted images: show

enlarged hyperintense right sided retropharyngeal lymph node which
showed restricted diffusion (green arrows).
61
Results
(F) Post-contrast sagittal T1w image: shows the enhancing pre-clival

nasopharyngeal mass (blue arrow) infiltrating into the clivus (red arrow)
with pre-pontine enhancing component (yellow arrow).
62
Results
Case 8:
(A)
(B)
(C)
(D)
63
Results
(E)
Fig. 35 Case 8: A 62 years old female patient of left sided

nasopharyngeal carcinoma
(A) Axial T2w image: shows a left sided iso-intense nasopharyngeal

mass lesion obliterating the left fossa of Rosenmller (orange arrow).
(B) Post-contrast axial T1w fat saturation image: shows superior

extension of the moderately enhancing tumor with total encasement of the
internal carotid artery (blue arrow).
(C) Post-contrast axial T1w fat saturation image: shows inferior

extension of the enhancing nasopharyngeal tumor along the lateral
pharyngeal wall reaching the oropharynx (red arrow).
(D and E) Pre-contrast sagittal T1w and post-contrast T1w fat

saturation images: shows hypo-intense infiltration of the tumor in the
bone marrow of the clivus with post contrast enhancement (yellow
arrow).
64
Results
Case 9:
(A)
(B)
(C)
(D)
65
Results
Fig. 36 Case 9: A 50 years old male patient with left sided

(A) Axial T2w image: shows a left sided isointense nasopharyngeal

mass lesion (white arrow) with anterior extension through the left choana
into the left nasal cavity (red arrow).
(B) Axial T1w image: The hypointense nasopharyngeal mass extends

anteriorly to the pterygopalatine fossa with obliteration of the
pterygopalatine fossa fat signal (orange arrow).
(C) Post-contrast sagittal T1w image: shows moderately enhancing

nasopharyngeal lesion (green arrow) with superior extension infiltrating
the clival marrow (yellow arrow) and the sphenoid sinus (blue arrow).
(D) Axial T2w image: shows a left sided lateral retropharyngeal

enlarged lymph node showing hyper-intense signal (red arrow).
66
Results
Case 10
(A)
(B)
(C)
(D)
67
Results
Fig. 37 Case 10: A 65 years old male patient of right sided

(A and B) Axial T2w and post-contrast T1w images: show a right

sided nasopharyngeal mass lesion showing T2 iso-intensity with
moderate post-contrast enhancement which infiltrates the levator veli
palatini and medial pterygoid muscles with obliteration of the
parapharyngeal fat (white arrow). The tumor infiltrates posteriorly the
anterior surface of the right prevertebral muscle (yellow arrow).
(C) Post-contrast axial T1w image: shows enhancing intracranial

extra-axial temporal component (red arrow).
(D) Post-contrast coronal T1w fat saturation image: The

moderately enhancing nasopharyngeal lesion (blue arrow) extends
superiorly through the right foramen ovale (black arrow) with intracranial
extra-axial component reaching the cavernous sinus and encasing the
internal carotid artery (red arrow).
68
Discussion
DISCUSSION
Nasopharyngeal carcinoma (NPC) is a rare malignancy in most parts
of the world, with an incidence well under 1 per 100,000 person-years.
Populations with elevated rates include the natives of Southeast Asia, the
natives of the Arctic region, and the Arabs of North Africa and parts of the
Middle East. (1)
The present study included 20 patients with pathologically proven
NPC as 12 (60%) males and 8 (40%) females with a mean age of 45.9 years.
Parkin DM et al (2002) stated that in almost all populations surveyed,
the incidence of NPC is 2- to 3-folds higher in males than in females.
(72)
In
our study, male to female ratio was of about 1.5 folds higher in males than in
females.
In most low-risk populations, NPC incidence increases monotonically
with increasing age.
(73-75)
In the contrary, in high-risk groups, the incidence
peaks around ages 50 to 59 years and declines thereafter.
(76, 77)
In our study,
patients age ranged from 24 to 65 years with bimodal peaks of 6 and 5 cases
for the 5th and 7th decades of life respectively.
Of the studied NPC cases, 8 cases (40%) were seen on the right side,
11 cases (55%) on the left side, and 1 case (5%) diffusely infiltrating both
sides and crossing the midline.
69
Discussion
Since NPC is diagnosed by endoscopy, the foremost role of CT or

MRI is to determine the extent of primary tumor and the presence of
metastatic adenopathy. (78)
Accurate assessment of the disease extent facilitates appropriate
treatment planning and prognosis. (79)
NPC is generally iso-dense to muscle on non-enhanced CT. It is
usually hypo- to iso-intense and relatively hyper-intense to muscles on T1weighted and T2-weighted MR images, respectively. Mild to moderate
tumor enhancement is evident following intravenous contrast injection on
both CT and MRI.
Ng SH et al (1997) stated that CT and MRI findings were essentially
in agreement in patients whose disease was limited to the nasopharyngeal
cavity, but not those with tumor spreading beyond the boundaries of the
nasopharynx. (80)
The pharyngobasilar fascia, the medial border of the parapharyngeal
space, is normally seen on MRI and not on CT. Involvement of the
parapharyngeal space denotes at least T2 stage of the tumor.
(81-84)
In NPC,
parapharyngeal space involvement can be assessed directly by MRI, which

shows tumor displacement or infiltration of the pharyngobasilar fascia or
extension through the sinus of Morgagni.
(81, 85)
In contrast, involvement of
the parapharyngeal space by CT is inferred indirectly by an abnormal soft

tissue deforming the parapharyngeal fibro-fatty tissue plane or by outward
bulging of an imaginary line between the medial pterygoid plate and the
lateral border of the carotid artery. (84, 86)
70
Discussion
In our study the involvement of the parapharyngeal space was

demonstrated in 7 cases by CT and in 8 cases by MRI. King AD et al (2000)
found that CT scanning suggested the presence of parapharyngeal tumor
extension more frequently than MRI because of its inability to distinguish
the primary tumor from lateral retropharyngeal nodes, and direct tumor
invasion of the parapharyngeal region from tumor compression.
(87)
Xie C et
al (2004) in a study on 69 patients found that there was no difference

between CT and MRI in demonstrating the invasion of the parapharyngeal
space. (88)
Further laterally, the tumor may spread into the masticator space.
Anatomic masticator space involvement affects the overall survival and local
relapse-free survival of patients with NPC. The frequency of masticator
space involvement in NPC is 19.7% as declared by Abdel Khalek Abdel
Razek A. et al (2012).
(89)
Infiltration of the medial and lateral pterygoid
muscles, infratemporal fat, and temporalis muscle is found when tumors

extend laterally from the parapharyngeal space, pterygoid base, or the
pterygo-maxillary fissure.
(66, 90)
When the muscles of mastication (notably
the medial and lateral pterygoid muscles) are involved, the patient often
complains of trismus (Chong VF 1997).
(91)
The mandibular nerve within the
masticator space may also be infiltrated, resulting in denervation atrophy of

the muscles of mastication. MRI features of denervation atrophy of these
muscles appear as T2 hyperintensity with asymmetrically reduced bulk of
the muscle of the affected side compared to the normal side (Chong VF et al
2008). (92)
In our study, the masticator space was involved in 3 cases (15%) and
it was as well seen in both CT and MRI. 2 cases showed involvement of the
71
Discussion
pterygoid fossa and the pterygo-maxillary fissure, and in the third one
showed denervation changes involving the ipsilateral masticator muscles,
sequel to mandibular nerve affection in the masticator space.
Further posterolateral spread may also involve the carotid space and
encase the carotid artery.
(93)
Carotid artery encasement is defined as tumor
tissue surrounding >270o of the vessel circumference.
(69)
This becomes
important in the follow-up setting, where surgical resection (e.g.

nasopharyngectomy or lymph node dissection) may be contemplated. The
patient is deemed inoperable if this is present, as the surgeon cannot remove
all the tumor tissue. Other potential issues that may result from encasement
include vascular invasion and potential carotid artery blow-outs postradiotherapy. Different criteria for detecting carotid artery involvement on
CT are suggested, and accordingly differs the sensitivity and accuracy in
detecting the vascular encasement. The use of loss of the fat plane between
the tumor and the carotid artery leads to very high false positive rates but
with a sensitivity of 100%.
(94-96)
Others, suggest the use of tumor in contact
with one-half of the circumference of the artery and loss of the tissue planes,
with a much less false positive rates.
(95, 97)
Other imaging characteristics are
carotid artery deformation, compression and segmental obliteration of the

fat.
Kraus DH et al (1992) declared that MRI was superior to CT in
determining carotid artery involvement.
(82)
Yousem DM et al (1995), in a
study of carotid artery encasement, sensitivity of MRI was 100% and

specificity 88%.
(98)
Sarvanan K et al (2002) studied encasement of >270
degrees and loss of fat planes. Sensitivity reached 75% and specificity
100%. (99)
72
Discussion
In our study we depicted only 1 case (5%) of carotid space

involvement by total encasement of the still patent carotid artery by NPC,
and that was seen by CT and by MRI as well.
In patients with NPC, paranasal sinuses involvement denotes a tumor
of at least stage T3. Paranasal sinus opacity is a common finding seen on
CT; it is occasionally difficult to differentiate whether it represents tumor
invasion or sinonasal secretions. On MRI, hydrated secretions within the
obstructed paranasal sinuses are of increased signal on T2-weighted images.
Thus, high-signal secretions can be differentiated from an intermediate
signal-intensity tumor.
(82)
Desiccated or mixed sinonasal secretions may
exhibit signal characteristics similar to those of tumor on both T1- and T2weighted images; contrast-enhanced MRI is then helpful because tumor
within the sinus enhances whereas sinonasal secretions do not enhance and
are surrounded by a rim of strongly enhancing sinus mucosa.
(100, 101)
In late
involvement of the sinuses, erosion of the sinus walls is a straightforward

exercise except in early cases. CT is superior to MRI in visualizing erosions
of paranasal sinuses floor. (53, 102)
In our study, we found that paranasal sinuses involvement was
demonstrated in the sphenoid sinus in 6 cases while in CT 4 cases showed
invasion of the sinus floor as erosions and the other 2 cases were equivocal
regarding the discrimination of the paranasal sinus secretions from tumor
tissue infiltration. The remaining 2 cases were only discriminated as
sphenoid sinus involvement in the enhanced MRI series. The maxillary sinus
involvement could be seen equally in CT and MRI in one case. In
agreement, Chong VF et al (1998) and Ng SH et al (1997) stated that
enhanced MRI excels on CT in detection and discrimination of involvement
73
Discussion
of NPC in the sphenoid and ethmoidal sinuses from inflammatory paranasal

secretions, and that both CT and MRI are equal in the detection and
discrimination of the tumor involvement of the maxillary sinus from
inflammatory secretions. (53, 80)
The significance of pterygopalatine fossa (PPF) involvement by
NPC is that once the tumor gains access to the pterygopalatine fossa, it gains
a route of spread to the orbit, infratemporal fossa, nasal cavity, and middle
cranial fossa. Earliest indication of tumor infiltration of the pterygopalatine
fossa is the replacement of the normal fat content. Widening of the fossa and
erosion of the bony margins are late signs. As expected, bony abnormality is
best seen on CT. However, direct visualization of tumor or replacement of
fat is more elegantly demonstrated on T1-weighted MRI. (103)
In our study, Pterygopalatine fossa invasion was demonstrated in 9
cases by MRI and by CT in 7 cases only and 2 cases were seen by MRI only
as obliteration of fossa fat signal by the tumor. This agrees with Tomura N.
et al (1999) where CT didnt depict the abnormalities in the pterygopalatine
fossa in five patients (17%) of a total of 30 patients with pterygopalatine
fossa involvement, while unenhanced T1w MR images depicted the tumoral
invasion in all patients.
(104)
In agreement, also Chong VF et al (1995 and
1997) stated that direct visualization of fat replacement by the tumor is

better seen on T1w images. (103, 105)
Detection of skull base bone involvement is based on either direct
visualization of tumor infiltration or detection of the reaction of bone to the
malignant process. MRI can identify early involvement of bone marrow. CT,
which depends mainly on bone destruction, provides detailed bone
74
Discussion
morphology. Both cortical and trabecular bone components are well defined
by CT. Based on the balance between the osteoclastic and osteoblastic
processes, the radiologic appearance of a bone involvement may be lytic,
sclerotic (blastic), or mixed. (106) Rapidly growing aggressive metastases tend
to be lytic, whereas sclerosis is considered to indicate a slower tumor growth
rate. Sclerosis may also be a sign of repair after treatment.
(107-109)
CT is not
sensitive for assessment of malignant marrow infiltration. (106, 110)

In NPC with skull base invasion, CT can directly determine the extent
of cortical bone destruction and/or remodeling by cancer.
(82, 85, 86, 111, 112)
On
the other hand, MRI can show tumor involvement of the skull base as a
lesion with different signal intensities encroaching on the signal-void bone
cortex or replacing the marrow. (82, 85) Contrast-enhanced fat-suppressed MRI
provides a better delineation of tumor extension into the clivus and allows
discrimination of tumor invasion from edema of the marrow. (113) The clivus,
pterygoid bones, body of the sphenoid and apices of the petrous temporal
bones are most commonly invaded. (114)
In our study skull base bony involvement was seen in 18 cases (90%)
by CT and in 17 cases (85%) by MRI. In 53 patients with NPC studied by
Olmi P et al, CT showed skull base erosion in 12 patients and MRI in 8.
(112)
Ng SH et al (1997) stated that skull base destruction was revealed in 27 of

67 cases (40.3 %) on CT and in 40 cases (59.7 %) on MRI, and that there
was no case in which the skull-base invasion was not visible on MRI, while
there were 13 cases (19.4 %) in which it was detected only by MRI.
(80)
CT demonstrated lytic bone invasion in 7 cases, while 8 cases were

seen by MRI. MRI, mainly the enhanced T1w fat suppressed images,
75
Discussion
excelled over CT and demonstrated 1 case of lytic infiltration of the skull

base bone that couldnt be seen by CT. In contrast, CT better demonstrated
sclerotic bone involvement in 5 cases but 3 cases were seen only by MRI.
We acknowledge that bone window CT excels over MRI in visualizing tiny
bony erosions by the tumor without involvement of the bone marrow. In
mixed sclerotic and erosive invasion of the bone, both CT and MRI
demonstrated 6 cases as well. To be noted that bone sclerosis alone, can be
either bone infiltration by osteoblastic tumor, or remodeling activity due to
nearby tumor.
The skull base foramina and fissures which include the foramen
rotundum (V2 nerve), the vidian canal (vidian nerve), the foramen ovale (V3
nerve), and foramen lacerum should be examined. The foramen ovale and
lacerum are common routes of tumor extension into the intracranial cavity.
(114)
Lederman M (1961) stated that foramen lacerum is the most frequently
invaded foramen due to its close proximity to the lateral pharyngeal recess.
(115)
While the skull base foramina present an unobstructed route for tumor
spread, direct invasion of the bone bordering these foramina is also a

common finding. The skull base foramina are best assessed on coronal
images. Less common findings include inferior spread of tumor to involve
the hypoglossal nerve canal (XII nerve) and jugular foramen (IX-XI nerves).
(114)
Nerves are resistant to tumor, and perineural tumor spread (PNS) is

an insidious and often asymptomatic process by which NPC can invade
upward and backward through the skull base to the cavernous sinus and
middle cranial fossa and invade CN II to VI (upper CN palsy). Cranial
nerves involvement indicates a tumor T-stage of T4. It may also involve the
76
Discussion
carotid space, where it may compress or invade CN XII as it exits through

the hypoglossal canal, CN IX to XI as they emerge from the jugular
foramen. (116, 117)
CN involvement on MRI is seen when there is asymmetric
enlargement, asymmetric enhancement on gadolinium-enhanced T1weighted images, obliteration of perineural fat planes, denervation changes
in end organs supplied by the nerves, and at last widening of foramina and
foraminal wall affection. (118, 119) Skip lesions may also be noted. (120)
Widening of a foramen or fissure that an involved nerve normally
traverses is an indirect sign of perineural spread, and this is best appreciated
on CT scan using bone algorithm. Features such as obliteration of juxtaforaminal fat pads and fat planes along the path of a CN are seen well on
both modalities. Expansion of the cavernous sinus and soft tissue
enhancement of Meckels cave, which is normally fluid filled, are other
indicators of PNS on CT and MRI. (118)
In our study, skull base foraminal involvement was seen by bone
algorithm CT and the enhanced MR T1w fat saturated images as well in 17
cases (85%). The foramen ovale was involved in 8 cases (40%), foramen
lacerum in 9 cases (45%), jugular foramen in 1 case (5%), sphenopalatine
foramen in 1 case (5%), and foramen rotundum in 1 case (5%). Of these 17
cases, only 11 (55%) cases showed perineural spread as demonstrated by
MRI, and 3 cases of perineural spread were missed by CT. Perineural spread
was seen along the mandibular nerve (CN V3) in 6 cases by MRI and of
these cases, one case was missed by CT. Maxillary (CN V 2) was involved in
3 cases by MRI, one of them was missed by CT. The vidian nerve
77
Discussion
involvement was demonstrated in 4 cases by MRI, while CT missed one

case. The facial nerve (CN VII) was involved in 1 case by MRI and was
missed in CT. Thus we declare that CT and MRI, especially the 3D gradientecho T1w post-contrast series, were as well in depicting the involvement of
the bony foramina, and MRI excelled over CT in detecting perineural
spread. In agreement, King AD et al (1999) acknowledged that perineural
spread would be underestimated unless enhanced fat saturated images are
obtained.
(121)
Maxillary and mandibular nerve involvement is best seen on
coronal T1-weighted contrast-enhanced MRI with fat saturation.
(118)
MRI is
generally more sensitive than CT in detecting all features of perineural

spread except for enlargement and destruction of bony foraminal boundaries.
Also Caldemeyer KS et al (1998), Liao XB et al (2008); Ng SH et al (2009),
Sakata K et al (1999) agreed in that MRI was superior in identifying
perineural spread. (122-125)
Intracranial extension occurs either from direct extension or through
skull base foramina (direct invasion, or perineural spread). Intracranial
extension denotes T4, stage IV tumors. Features denoting intracranial
extension include cavernous sinus involvement, meningeal involvement
(especially if seen as nodular enhancing masses), and less frequently masses
within the middle and/or posterior cranial fossa, respectively according to
the frequency of involvement.
(69, 79)
Anterior cranial fossa invasion by NPC
is rarely seen. To be noted that posterior cranial fossa is seen more readily
with MRI due to its pluri-directional scanning and does not show beamhardening artifact from the dense bone of the skull base.
(80)
In our study, intracranial extension was detected by CT in 7 cases

(35%) and by MRI in 8 cases (40%). MRI excelled over CT in detection of
78
Discussion
intracranial extension in one case, where minor meningeal involvement was

seen in contrast enhanced T1w MR images. All of the studies we could
reach highlighted the superiority of MRI over CT, revealing intracranial
invasion, especially in conjunction with the contrast-enhanced fatsuppression technique. (69, 78, 82, 85, 113, 123, 126-129)
Nasopharyngeal carcinoma tumor may infiltrate submucosally
inferiorly to involve the oropharynx or even the hypopharynx. On imaging,
oropharyngeal extension is readily noted on coronal or sagittal MR
imaging as tumor that has extended inferiorly past the plane of palate. On
axial sections, the oropharynx is considered involved when tumor is seen
inferior to the C1/C2 junction. (66, 120)
In our study, MRI excelled over CT in detection of oropharyngeal
infiltration by NPC. Oropharyngeal carcinoma involvement was seen in 7
cases (35%) by CT. By MRI, 2 cases of these 7 cases seen by CT were
interpreted to be retropharyngeal lymph nodal involvement rather than true
oropharyngeal tumoral involvement. MRI detected 7 cases (35%) of
oropharyngeal infiltration by the nasopharyngeal carcinoma. Soft palate was
involved in 2 case, 3 cases showed creeping on the posterior and lateral
walls of the naso- and oro-pharynx, and 2 cases showed palatine tonsils and
pillars involvement. Retropharyngeal lymph nodal involvement in the
retropharyngeal space can be misinterpreted by CT as oropharyngeal
posterior and/or lateral walls involvement as described formerly. In
agreement, Ng SH (1997) in a study, Of 18 patients, in whom CT suggested
oropharyngeal involvement, seven actually had retropharyngeal adenopathy
disclosed by MRI, with subsequent down-staging of the cases.
(80)
Although
MR was better in the assessment of the oropharynx, the exam can be non79
Discussion
diagnostic secondary to excessive swallowing artifact, which is not

uncommon if the patient has pooling of saliva and a large tumor. (130) On the
other side, MRI avoids CTs dental amalgam artifact. (131)
Lymphadenopathy has very important prognostic implications. Up to
60-90% of NPC patients will have nodal metastases at presentation
(Glastonbury, 2007; Goh and Lim, 2009). (69, 132) Positive neck nodal disease
in NPC is associated with an increased risk of local recurrence and distant
metastases (Goh and Lim, 2009).
(69)
The presence of a single nodal
metastasis reduces the patients survival rate by 50%.
Bilateral
lymphadenopathy further reduces the survival rate by another 50%. Patients

with nodes showing necrosis and extra-nodal spread and fixation have a very
poor prognosis with a further 50% decreased 5-years survival rate. (130, 133, 134)
NPC generally follows a very orderly pathway of nodal spread,
beginning with the lateral retropharyngeal lymph nodes (RPLN) - located
medial to the carotid artery - before involving the nodal groups along the
internal jugular chain (levels II to IV), spinal accessory chain (Va and Vb),
as well as supraclavicular nodes (Glastonbury C, 2007; King AD et al,
2004).
(132, 135)
Nodal disease in the submandibular and parotid/periparotid
regions is a rare occurrence (Chong & Fan, 2000; King & Bhatia, 2010)
136)
(114,
Although the RPLN are generally considered the first echelon of
metastatic spread, studies have shown that this is not true in all cases and
that RPLN may be bypassed allowing direct spread to level IIa and IIb
nodes, which are the most common site for non-retropharyngeal nodal
involvement (Liu et al, 2006; Mao et al, 2008; Ng et al, 2004; Wang et al,
2009; King et al, 2000 and 2004).
(135, 137-141)
As medial retropharyngeal
nodes are usually not visible, any medial retropharyngeal nodes detected on
80
Discussion
MRI are highly suspicious of metastatic involvement (Wang et al, 2009).

(142)
In addition, Ng SH et al also reported skip metastases in the lower neck
lymph nodes and the supraclavicular fossa, and distant metastases to thoracic
and abdominal nodes. (137)
Several criteria are used in the evaluation of lymph nodes. Size is the
most commonly used. The measurements are taken using the shortest transaxial diameter and are considered suspicious when the shortest axis is >5
mm for RPLN, >1.5 cm for levels I and II, and >1 cm for levels IV-VII (Goh
and Lim, 2009; King and Bhatia, 2010). (69, 114)
A cluster of 3 or more lymph nodes borderline in size, rounded nodes
with loss of the fatty hilum, and necrosis are also suggestive of metastatic
disease (King and Bhatia, 2010).
(114)
However, nodes may still be of normal
size and harbor malignant cells. The ratio of the longest longitudinal to axial
dimensions has also been proposed; if the ratio is less than 2, this
suggests metastatic carcinoma. Normal nodes should have a ratio greater
than 2. (69)
If identified, necrosis is considered 100% specific. However, due to
resolution restrictions, necrosis can only be reliably identified in tumor foci
greater than 3 mm, of which approximately one-third reportedly have nodal
necrosis (Goh and Lim, 2009; Som and Brandwein, 2003; Yousem et al,
1992).
(69, 143, 144)
Necrosis or cystic change is hypo-intense on T1-weighted
images with rim enhancement after contrast injection, and hyper-intense on

T2-weighted images. In CT images, necrosis is seen as a focal area of hypoattenuation with or without post-contrast rim enhancement. (110)
81
Discussion
In extra-nodal spread, there is extension beyond the capsule into the

adjacent soft tissues. It is recognized radiologically as loss or irregularity of
the nodal margins, and/or streakiness of the adjacent fat, although the latter
may occur in the context of inflammation.
(145)
Invasion of adjacent
structures may occur, for example, sternocleidomastoid muscle or carotid

artery encasement.
(69)
The fat-suppression technique, in conjunction with
T2-weighted and contrast-enhanced T1-weighted images, facilitates the

detection of lymphadenopathy and the presence of nodal necrosis or extracapsular nodal spread. (81, 113, 146, 147)
Retropharyngeal lymph nodes involvement denotes at least N1 stage
when involved by the NPC. Metastatic lateral retropharyngeal nodes can be
identified from the skull base to the level of C3. (148)
In our study MRI allowed better detection of retropharyngeal nodal
metastases than CT (8 cases versus 4). In the 4 cases in which
retropharyngeal adenopathy were recognized only on MRI, 1 case had been
misinterpreted on CT as retropharyngeal tumor extension and as nodal
negative. In this case, MRI only demonstrated the positive nodal
involvement and was negative by CT. In agreement, Ng SH et al (1997)
found that MRI detected retropharyngeal space in 39 cases of 67 cases while
CT demonstrated only in 14 cases with the remainder 25 cases were
misinterpreted as oropharyngeal or carotid space involvement.
(80)
Abdel
Khalek Abdel Razek A. et al (2011), King AD et al (2000), King AD et al

(2008), Chang JT et al (2005), Chong VF et al (1996), and Chung NN et al
(2004) also agreed in that MRI has an advantage over CT in being better
able to separate the lateral retropharyngeal nodes from the primary tumor in
82
Discussion
the adjacent posterolateral nasopharynx because of its better discrimination

of nodes. (128, 139, 148-151)
In our study, cervical metastatic lymph nodal involvement else than
lateral retropharyngeal lymph nodes were seen in 15 cases (75%) as well in
CT and MRI, with both modalities identifying nodal necrosis and extracapsular extension as well in 5 cases (25%) for nodal necrosis and in 3 cases
(15%) for the extra-capsular extension. Ng SH et al (1997), in a study on 67
cases, MRI detected more cervical lymph nodes than CT in 3 cases.
(80)
In
agreement, King AD et al (2004) found both techniques to be comparable,

with an accuracy of 92% versus 91% for CT and MRI, respectively.
(135)
Also, Liao XB et al (2008) stated that the incidence of cervical lymph node
metastasis at each level of non-retropharyngeal cervical lymph nodes was
similar according to CT and MRI. (123) Stambuk HE and Fischbein NJ (2008)
stated that extra-capsular extension is demonstrated earlier on CT compared
to MRI.
(130)
Yu E et al (2010) stated that the high resolution CT facilitates
the visualization of cervical lymph adenopathy as well as nodal necrosis and

extra-capsular extension. (145)
83
Summary
SUMMARY
Nasopharyngeal carcinoma is a rare malignancy with a characteristic
geographic and ethnic distribution. It mostly arises from the lateral
nasopharyngeal fossa of Rosenmller and spreads widely into the
surroundings along well-defined routes.
The present study included 20 cases of pathologically proven
nasopharyngeal carcinoma. Multi-detector CT especially bone algorithm
and MRI as well as post-contrast studies were done and reviewed
regarding the value of both modalities in the detection and staging of the
disease, which affect the therapeutic planning and prognosis.
The role of radiological assessment of the nasopharyngeal tumors is
correct staging of the disease and hence treatment planning and
administration.
CT and MRI are in agreement in patients with disease limited to the
nasopharyngeal mucosal space.
MRI excelled over CT in demonstrating the parapharyngeal,
oropharyngeal and carotid spaces involvement by accurate visualization
of the tumor extension and discriminating the true tumor involvement
from the retropharyngeal lymph nodal invasion that maybe misinterpreted
by CT.
MRI and CT showed the extension of the tumor to the masticator
space equally with better demonstration of mandibular nerve involvement
in the space (perineural spread) by MRI.
84
Summary
In paranasal sinuses involvement, MRI was better than CT in

discrimination between nasopharyngeal carcinoma invasion of the sinuses
from dehydrated inflammatory sinonasal secretions by contrast enhanced
MRI. CT was better in visualizing sphenoid sinus floor erosion.
Pterygopalatine fossa assessment is critical as it is a station where
the tumor can gain access to intracranial cavity, orbit, nasal cavity and
infratemporal fossa. T1 weighted MR images excelled in direct
visualization of the pterygopalatine fossa invasion by the tumor and CT
better visualized the bony erosions of its boundaries.
Contrast enhanced fat-suppressed MRI excelled over CT in
detecting lytic and mixed bony involvement, while CT is better in
detecting sclerotic bone involvement which can be either infiltration of
bone by osteoblastic tumor or remodeling by a nearby neoplastic or
inflammatory process.
Skull base foramina and fissures were seen as well in CT bone
window algorithm and MR T1 fat-suppressed images. MRI especially the
3D gradient echo T1w post-contrast and fat-suppressed sequences
excelled over CT in demonstrating the perineural spread.
We demonstrated the superiority of MRI over CT in detecting
intracranial extension especially the contrast enhanced fat-suppressed
technique.
85
Summary
Metastatic lymphadenopathy is evaluated based on several criteria

including size, clustering, necrosis and extra-capsular extension. CT and
MRI performed as well in the assessment of the non-retropharyngeal
cervical lymph nodes. MRI excelled over CT in demonstrating lateral
retropharyngeal nodal involvement and differentiating the nodal
involvement from the direct extension of the tumor to the parapharyngeal,
oropharyngeal, and carotid spaces.
86
Conclusion
CONCLUSION
Head and neck MRI, due to its superior soft tissue contrast and
resolution is the best modality for staging loco-regional NPC, and the
common sites for local primary tumor invasion and patterns of nodal
spread. CT better visualized sclerotic bony involvement and tiny erosions
of the base of the skull.
87
References
References
1.
Chang ET, Adami HO. The enigmatic epidemiology of nasopharyngeal
carcinoma. Cancer Epidemiology Biomarkers & Prevention. 2006;15(10):1765-77.

2.
Proceedings of the IARC Working Group on the Evaluation of Carcinogenic
Risks to Humans. Epstein-Barr Virus and Kaposi's Sarcoma Herpesvirus/Human

Herpesvirus 8. Lyon, France, 17-24 June 1997. IARC monographs on the
evaluation of carcinogenic risks to humans / World Health Organization,
International Agency for Research on Cancer. 1997;70:1-492.
3.
Zong YS, Sham JS, Ng MH, Ou XT, Guo YQ, Zheng SA, Liang JS, Qiu H.
Immunoglobulin A against viral capsid antigen of Epstein-Barr virus and indirect

mirror examination of the nasopharynx in the detection of asymptomatic
nasopharyngeal carcinoma. Cancer. 1992;69(1):3-7.
4.
Zeng Y, Zhang LG, Li HY, Jan MG, Zhang Q, Wu YC, Wang YS, Su GR.
Serological mass survey for early detection of nasopharyngeal carcinoma in

Wuzhou City, China. International Journal of Cancer. 1982;29(2):139-41.
5.
Zeng Y, Liu YX, Wei JN, Zhu JS, Cai SL, Wang PZ, Zhong JM, Li RC, Pan
WJ, Li EJ, Tan BF. Serological mass survey of nasopharyngeal carcinoma

(author's transl). Zhongguo yi xue ke xue yuan xue bao. Acta Academiae
Medicinae Sinicae. 1979;1(2):123.
6.
Zeng Y, Zhang L, Wu Y, Huang Y, Huang N, Li J, Wang YB, Jiang
MK, Fang Z, Meng NN. Prospective studies on nasopharyngeal carcinoma in
88
References
epsteinbarr virus IgA/VCA antibodypositne persons in Wuzhou city, china.

International journal of cancer. 1985;36(5):545-7.
7.
Zeng Y, Zhong JM, Li LY, Wang PZ, Tang H, Ma YR, Zhu JS, Pan WJ, Liu
YX, Wei ZN. Follow-up studies on EpsteinBarr virus IgA/VCA antibody-positive

persons in Zangwu County, China. Intervirology. 1983;20(4):190-4.
8.
Deng H, Zeng Y, Lei Y, Zhao Z, Wang P, Li B, Pi Z, Tan B, Zheng Y, Pan
W. Serological survey of nasopharyngeal carcinoma in 21 cities of south China.

Chinese medical journal. 1995;108(4):300.
9.
Farrow DC, Vaughan TL, Berwick M, Lynch CF, Swanson GM, Lyon JL.
Diet and nasopharyngeal cancer in a lowrisk population. International journal of

cancer. 1998;78(6):675-9.
10.
Vaughan TL, Shapiro JA, Burt RD, Swanson GM, Berwick M, Lynch CF,
Lyon JL. Nasopharyngeal cancer in a low-risk population: defining risk factors by

histological type. Cancer Epidemiology Biomarkers & Prevention. 1996;5(8):58793.
11.
Zhu K, Levine RS, Brann EA, Hall HI, Caplan LS, Gnepp DR. Casecontrol
study evaluating the homogeneity and heterogeneity of risk factors between

sinonasal and
nasopharyngeal cancers.
International journal
of cancer.
2002;99(1):119-23.
12.
Yuan JM, Wang XL, Xiang YB, Gao YT, Ross RK, Yu MC. Nondietary
risk factors for nasopharyngeal carcinoma in Shanghai, China. International journal

of cancer. 2000;85(3):364-9.
89
References
13.
Mirabelli MC, Hoppin JA, Tolbert PE, Herrick RF, Gnepp DR, Brann EA.
Occupational exposure to chlorophenol and the risk of nasal and nasopharyngeal

cancers among US men aged 30 to 60. American journal of industrial medicine.
2000;37(5):532-41.
14.
Zhu K, Levine R, Brann E, Gnepp D, Baum M. Cigarette smoking and
nasopharyngeal cancer: an analysis of the relationship according to age at starting

smoking and age at diagnosis. Journal of epidemiology/Japan Epidemiological
Association. 1997;7(2):107-11.
15.
West S, Hildesheim A, Dosemeci M. Nonviral risk factors for
nasopharyngeal carcinoma in the philippines: Results from a casecontrol study.

16.
Chow WH, McLaughlin JK, Hrubec Z, Nam JM, Blot WJ. Tobacco use and
nasopharyngeal carcinoma in a cohort of US veterans. International journal of

cancer. 1993;55(4):538-40.
17.
Nam JM, McLaughlin JK, Blot WJ. Cigarette smoking, alcohol, and
nasopharyngeal carcinoma: a case-control study among US whites. Journal of the

National Cancer Institute. 1992;84(8):619-22.
18.
Yu MC, Garabrant DH, Huang TB, Henderson BE. Occupational and other
nondietary risk factors for nasopharyngeal carcinoma in Guangzhou, China.

International Journal of Cancer. 1990;45(6):1033-9.
19.
Mabuchi K, Bross DS, Kessler II. Cigarette smoking and nasopharyngeal
carcinoma. Cancer. 1985;55(12):2874-6.
90
References
20.
Lin
TM, Chen
KP, Lin
CC, Hsu
MM, Tu
SM, Chiang
TC, Jung
PF, Hirayama T. Retrospective study on nasopharyngeal carcinoma. Journal of the

National Cancer Institute. 1973;51(5):1403-8.
21.
Armstrong RW, Armstrong MJ, Mimi CY, Henderson BE. Salted fish and
inhalants as risk factors for nasopharyngeal carcinoma in Malaysian Chinese.

Cancer research. 1983;43(6):2967-70.
22.
Henderson BE, Louie E, Jing JS, Buell P, Gardner MB. Risk factors
associated with nasopharyngeal carcinoma. New England Journal of Medicine.

1976;295(20):1101-6.
23.
Jung P. Familial tendency of nasopharyngeal carcinoma; a report of cases.
Pacific medicine and surgery. 1965;73:242-3.

24.
Gajwani B, Devereaux J, Beg J. Familial clustering of nasopharyngeal
carcinoma. Cancer. 1980;46(10):2325-7.

25.
Zhang F, Zhang J. Clinical hereditary characteristics in nasopharyngeal
carcinoma through Ye-Liang's family cluster. Chinese medical journal.

1999;112(2):185-7.
26.
Loh KS, Goh BC, Lu J, Hsieh W-S, Tan L. Familial nasopharyngeal
carcinoma in a cohort of 200 patients. Archives of OtolaryngologyHead & Neck

Surgery. 2006;132(1):82-5.
27.
Williams E. de The G (1974) Letter: familial aggregation in nasopharyngeal
carcinoma. Lancet.2(7875):295-6.
91
References
28.
Lanier AP, Bender TR, Tschopp CF, Dohan P. Nasopharyngeal carcinoma
in an Alaskan Eskimo family: report of three cases. Journal of the National Cancer
Institute. 1979;62(5):1121-4.
29.
Ireland B, Lanier Ap, Knutson L, Clift Se, Harpster A. Increased risk of
cancer in siblings of Alaskan native patients with nasopharyngeal carcinoma.

International journal of epidemiology. 1988;17(3):509-11.
30.
Albeck H, Bentzen J, Ockelmann HH, Nielsen NH, Bretlau P, Hansen H.
Familial clusters of nasopharyngeal carcinoma and salivary gland carcinomas in

Greenland natives. Cancer. 1993;72(1):196-200.
31.
Bell R, Maguda T. Nasopharyngeal carcinoma in Caucasian siblings: report
of two cases. Journal of the Tennessee Medical Association. 1970;63(9):753-4.

32.
Nevo S, Meyer W, Altman M. Carcinoma of nasopharynx in twins. Cancer.
1971;28(3):807-9.
33.
Snow Jr J. Carcinoma of the nasopharynx in children. The Annals of
otology, rhinology, and laryngology. 1975;84(6):817-26.

34.
Brown TM, Heath CW, Lang R, Lee S, Whalley B. Nasopharyngeal cancer
in Bermuda. Cancer. 1976;37(3):1464-8.

35.
Joncas J, Rioux E, Wastiaux J, Leyritz M, Robillard L, Menezes J.
Nasopharyngeal carcinoma and Burkitt's lymphoma in a Canadian family. I. HLA

typing, EBV antibodies and serum immunoglobulins. Canadian Medical
Association Journal. 1976;115(9):858-60.
92
References
36.
Fischer A, Fischer G, Cooper E. Familial nasopharyngeal carcinoma.
Pathology. 1984;16(1):23-4.
37.
Schimke RN, Collins D, Cross D, Opitz JM, Reynolds JF. Nasopharyngeal
carcinoma, aplastic anemia, and various malignancies in a family: Possible role of

EpsteinBarr virus. American journal of medical genetics. 1987;27(1):195-202.
38.
Coffin CM, Rich SS, Dehner LP. Familial aggregation of nasopharyngeal
carcinoma and other malignancies. A clinicopathologic description. Cancer.

1991;68(6):1323-8.
39.
Levine PH, Pocinki AG, Madigan P, Bale S. Familial nasopharyngeal
carcinoma in patients who are not Chinese. Cancer. 1992;70(5):1024-9.

40.
Shepstone B. Anatomy for Diagnostic Imaging. Journal of Anatomy.
2004;205(2):157.
41.
Harnsberger HR, Macdonald AJ. Diagnostic and surgical imaging anatomy:
brain, head & neck, spine: Amirsys Salt Lake City; 2006.
42.
Ryan S, Mcnicolas M, Eustace S. Anatomy for diagnostic imaging. 2003.
43.
Sinnatamby CS. Last's anatomy: regional and applied: Elsevier Health
Sciences; 2011.
44.
Gaillard F. prominent adenoids in child: Radiopedia; 2009. Available from:
http://radiopaedia.org/images/25041.
45.
Standring S. Gray's anatomy. 2008.
93
References
46.
Som PM, Curtin HD, Mancuso AA. Imaging-based nodal classification for
evaluation of neck metastatic adenopathy. American Journal of Roentgenology.

2000;174(3):837-44.
47.
Som PM, Curtin HD, Mancuso AA. An imaging-based classification for the
cervical nodes designed as an adjunct to recent clinically based nodal

classifications.
Archives
of
OtolaryngologyHead
&
Neck
Surgery.
1999;125(4):388-96.
48.
Ryan S, McNicholas M, Eustace SJ. Anatomy for diagnostic imaging:
Saunders Elsevier; 2011.

49.
Gates GA. Sizing up the adenoid. Archives of OtolaryngologyHead &
Neck Surgery. 1996;122(3):239-40.

50.
Som PM, Curtin HD. Head and neck imaging: Mosby Elsevier Health
Science; 1996.
51.
Yousem DM, Loevner LA, Tobey JD, Geckle RJ, Bilker WB, Chalian AA.
Adenoidal width and HIV factors. American journal of neuroradiology.

1997;18(9):1721-5.
52.
Harnsberger HR, Osborn AG. Differential diagnosis of head and neck
lesions based on their space of origin. 1. The suprahyoid part of the neck. AJR
American journal of roentgenology. 1991;157(1):147-54.
53.
Chong VF, Fan YF, Khoo JB. Computed tomographic and magnetic
resonance imaging findings in paranasal sinus involvement in nasopharyngeal

carcinoma. Ann Acad Med Singapore. 1998;27(6):800-4.
94
References
54.
Baum U, Greess H, Lell M, Nmayr A, Lenz M. Imaging of head and neck
tumorsmethods: CT, spiral-CT, multislice-spiral-CT. European journal of

radiology. 2000;33(3):153-60.
55.
Som PM, Curtin HD. Head and neck imaging: Elsevier Health Sciences;
2011.
56.
Butler P, Mitchell AW, Ellis H. Applied radiological anatomy for medical
students: Cambridge University Press; 2007.

57.
Wei K, Xu Y, Liu J, Zhang W, Liang Z. Histopathological classification of
nasopharyngeal carcinoma. Asian Pac J Cancer Prev. 2011;12(5):1141-7.

58.
Barnes L, Eveson J, Reichart P, Sidransky D. World Health Organization
Classification of Tumours: Pathology and Genetics of Head and Neck Tumours.

Lyon: IARC Press; 2005.
59.
Shanmugaratnam K, Sobin LH. The World Health Organization histological
classification of tumours of the upper respiratory tract and ear. Cancer.

1993;71(8):2689-97.
60.
Chan J, Pilch B, Kuo T, Wenig B, Lee A. Tumors of the nasopharynx:
introduction in Pathology and Genetics of Head and Neck Tumours (World Health
Organization Classification of Tumours), L. Barnes, JW Eveson, P. Reichart, and
D. Sidransky, Eds. IARC press, Lyon, France; 2005.
61.
Pizzo PA, Poplack DG. Principles and Practice of Pediatric Oncology.
Journal of the American College of Surgeons. 1997;185(2):203-4.
95
References
62.
Neel 3rd H, Pearson G, Taylor W. Antibodies to Epstein-Barr virus in
patients with nasopharyngeal carcinoma and in comparison groups. The Annals of

otology, rhinology, and laryngology. 1984;93(5 Pt 1):477-84.
63.
Edge S, Fritz A, Byrd D, Greene F, Compton C, Trotti A. Pharynx
(Including Base of Tongue, Soft Palate, and Uvula) AJCC Cancer Staging manual.
New York: Springer; 2010.
64.
Edge SB, Compton CC. The American Joint Committee on Cancer: the 7th
edition of the AJCC cancer staging manual and the future of TNM. Annals of
surgical oncology. 2010;17(6):1471-4.
65.
Krueger G, Wustrow J. Current histological classification of nasopharyngeal
carcinoma (NPC) at Cologne University. Nasopharyngeal carcinoma. 1981:11-5.

66.
Dubrulle F, Souillard R, Hermans R. Extension patterns of nasopharyngeal
carcinoma. European radiology. 2007;17(10):2622-30.

67.
Chong VF. Neoplasms of the nasopharynx.
Head and Neck Cancer
Imaging: Springer; 2006. p. 143-62.

68.
Roh J-L, Sung M-W, Kim KH, Choi BY, Oh SH, Rhee CS, Ha JW.
Nasopharyngeal carcinoma with skull base invasion: a necessity of staging

subdivision. American journal of otolaryngology. 2004;25(1):26-32.
69.
Goh J, Lim K. Imaging of nasopharyngeal carcinoma. Ann Acad Med
Singapore. 2009;38(9):809-16.
70.
Shanmugaratnam K, Sobin LH. Histological typing of upper respiratory tract
tumours. 1978.
96
References
71.
Forastiere
AA, Ang
K, Brizel
D, Brockstein
BE, Dunphy
F, Eisele
DW, Goepfert H, Hicks WL Jr, Kies MS, Lydiatt WM, Maghami E, McCaffrey
T, Mittal BB, Pfister DG, Pinto HA, Posner MR, Ridge JA, Samant S, Schuller
DE, Shah JP, Spencer S, Trotti A 3rd, Wheeler RH 3rd, Wolf GT, Worden F, Yueh
B. Head and neck cancers. Journal of the National Comprehensive Cancer Network
: JNCCN. 2005;3(3):316-91.
72.
Parkin D, Whelan S, Ferlay J, Teppo L, Thomas D. Cancer incidence in five
continents Vol. VIII. IARC scientific publications. 2002;155.

73.
Levine PH, Connelly RR, Easton JM. Demographic patterns for
nasopharyngeal carcinoma in the United States. International Journal of Cancer.

1980;26(6):741-8.
74.
Burt RD, Vaughan TL, McKnight B. Descriptive epidemiology and survival
analysis of nasopharyngeal carcinoma in the United States. International journal of

cancer. 1992;52(4):549-56.
75.
Lee JT, Ko CY. Has survival improved for nasopharyngeal carcinoma in the
United States? Otolaryngology--Head and Neck Surgery. 2005;132(2):303-8.

76.
Zong Y, Zhang R, He S, Qiu H. Histopathologic types and incidence of
malignant nasopharyngeal tumors in Zhongshan County. Chinese medical journal.

1983;96(7):511-6.
77.
Lee AW, Foo W, Mang O, Sze W, Chappell R, Lau W, Ko, WM. Changing
epidemiology of nasopharyngeal carcinoma in Hong Kong over a 20year period

(198099): An encouraging reduction in both incidence and mortality.
97
References
78.
Foust R, Duong R. Roles of computed tomography and magnetic resonance
imaging diagnoses in the treatment of head and neck cancer. Hematology/oncology

clinics of North America. 1991;5(4):657-65.
79.
Teo P, Shiu W, Leung S, Lee W. Prognostic factors in nasopharyngeal
carcinoma investigated by computer tomographyan analysis of 659 patients.

Radiotherapy and Oncology. 1992;23(2):79-93.
80.
Ng S-H, Chang T, Ko S, Yen P, Wan Y, Tang L, Tsai MH. Nasopharyngeal
carcinoma: MRI and CT assessment. Neuroradiology. 1997;39(10):741-6.

81.
Vogl T, Dresel S, Bilaniuk L, Grevers G, Kang K, Lissner J. Tumors of the
nasopharynx and adjacent areas: MR imaging with Gd-DTPA. AJR American

journal of roentgenology. 1990;154(3):585-92.
82.
Kraus DH, Lanzieri CE, Wanamaker JR, Little JR, Lavertu P.
Complementary use of computed tomography and magnetic resonance imaging in

assessing skull base lesions. The Laryngoscope. 1992;102(6):623-9.
83.
Teresi LM, Lufkin RB, Vinuela F, Dietrich R, Wilson G, Bentson J, Hanafee
WN. MR imaging of the nasopharynx and floor of the middle cranial fossa. Part I.
Normal anatomy. Radiology. 1987;164(3):811-6.
84.
Cheung Y, Sham J, Chan F, Leong L, Choy D. Computed tomography of
paranasopharyngeal spaces: normal variations and criteria for tumour extension.

Clinical radiology. 1992;45(2):109-13.
85.
Teresi L, Lufkin R, Vinuela F, Dietrich R, Wilson G, Bentson J, Hanafee
WN. MR imaging of the nasopharynx and floor of the middle cranial fossa. Part II.
Malignant tumors. Radiology. 1987;164(3):817-21.
98
References
86.
Sham J, Cheung Y, Choy D, Chan F, Leong L. Nasopharyngeal carcinoma:
CT evaluation of patterns of tumor spread. American journal of neuroradiology.

1991;12(2):265-70.
87.
King A, Teo P, Lam W, Leung S, Metreweli C. Paranasopharyngeal space
involvement in nasopharyngeal cancer: Dectection by CT and MRI. Clinical

Oncology. 2000;12(6):397-402.
88.
Xie C, Liang B, Lin H, Wu P. Influence of the application of MRI on the T,
N staging system of nasopharyngeal carcinoma. Chinese Journal of Clinical

Oncology. 2004;1(5):348-53.
89.
Abdel Khalek Abdel Razek A, King A. MRI and CT of Nasopharyngeal
Carcinoma. American Journal of Roentgenology. 2012;198(1):11-8.

90.
Tang L-L, Li W-F, Chen L, Sun Y, Chen Y, Liu L-Z, Mao YP, Lin AH, Li
L, Ma J. Prognostic Value and Staging Categories of Anatomic Masticator Space

Involvement in Nasopharyngeal Carcinoma: A Study of 924 Cases with MR
Imaging. Radiology. 2010;257(1):151-7.
91.
Chong V. Masticator space in nasopharyngeal carcinoma. The Annals of
otology, rhinology, and laryngology. 1997;106(11):979-82.

92.
Chong VF, Ong CK. Nasopharyngeal carcinoma. European journal of
radiology. 2008;66(3):437-47.
93.
Ng WT, Chan SH, Lee AW, Lau KY, Yau TK, Hung WM, Lee MC, Choi
CW. Parapharyngeal extension of nasopharyngeal carcinoma: still a significant

factor in era of modern radiotherapy? International Journal of Radiation Oncology,
Biology, Physics. 2008;72(4):1082-9.
99
References
94.
Reilly MK, Perry MO, Netterville JL, Meacham PW. Carotid artery
replacement in conjunction with resection of squamous cell carcinoma of the neck:

preliminary results. Journal of vascular surgery. 1992;15(2):324-30.
95.
Rothstein SG, Persky MS, Horii S. Evaluation of malignant invasion of the
carotid artery by CT scan and ultrasound. The Laryngoscope. 1988;98(3):321-4.

96.
Zaragoza L, Sendra F, Solano J, Garrido V, Martinez-Morillo M.
Ultrasonography is more effective than computed tomography in excluding

invasion of the carotid wall by cervical lymphadenopathies. European journal of
radiology. 1993;17(3):191-4.
97.
Takashima S, Morimoto S, Ikezoe J, Takai S, Kobayashi T, Koyama H,
Nishiyama K, Kozuka T. CT evaluation of anaplastic thyroid carcinoma.

American Journal of Roentgenology. 1990;154(5):1079-85.
98.
Yousem DM, Hatabu H, Hurst RW, Seigerman HM, Montone KT,
Weinstein GS, Hayden RE, Goldberg AN, Bigelow DC, Kotapka MJ. Carotid
artery invasion by head and neck masses: prediction with MR imaging. Radiology.
1995;195(3):715-20.
99.
Sarvanan K, Bapuraj JR, Sharma SC, Radotra BD, Khandelwal N, Suri S.
Computed tomography and ultrasonographic evaluation of metastatic cervical

lymph nodes with surgicoclinicopathologic correlation. The Journal of laryngology
and otology. 2002;116(3):194-9.
100. Crawford S, Harnsberger H, Lufkin R, Hanafee W. The role of gadoliniumDTPA in the evaluation of extracranial head and neck mass lesions. Radiologic
clinics of North America. 1989;27(2):219-42.
100
References
101. Mossa-Basha M, Blitz AM, editors. Imaging of the paranasal sinuses.

Seminars in roentgenology; 2013.
102. Chong VF, Fan YF. Skull base erosion in nasopharyngeal carcinoma:
detection by CT and MRI. Clin Radiol. 1996;51(9):625-31.
103. Chong VF, Fan YF, Khoo JB, Lim TA. Comparing computed tomographic
and magnetic resonance imaging visualisation of the pterygopalatine fossa in
nasopharyngeal carcinoma. Ann Acad Med Singapore. 1995;24(3):436-41.
104. Tomura N, Hirano H, Kato K, Takahashi S, Sashi R, Tate E, Watanabe
O, Okane K, Watarai J. Comparison of MR imaging with CT in depiction of
tumour extension into the pterygopalatine fossa. Clin Radiol. 1999;54(6):361-6.
105. Chong VF, Fan YF. Pterygopalatine fossa and maxillary nerve infiltration in
nasopharyngeal carcinoma. Head & neck. 1997;19(2):121-5.
106. Even-Sapir E. Imaging of malignant bone involvement by morphologic,
scintigraphic, and hybrid modalities. Journal of nuclear medicine : official
publication, Society of Nuclear Medicine. 2005;46(8):1356-67.
107. Padhani A, Husband J. Bone metastases. Imaging in Oncology Oxford, UK:
Isis Medical Media Ltd. 1998:765-87.
108. Blake GM, Park-Holohan S-J, Cook GJR, Fogelman I. Quantitative studies
of bone with the use of 18 F-fluoride and 99m Tc-methylene diphosphonate. Seminars
in Nuclear Medicine. 2001;31(1):28-49.
101
References
109. Bellamy EA, Nicholas D, Ward M, Coombes R, Powles T, Husband JE.

Comparison of computed tomography and conventional radiology in the
assessment of treatment response of lytic bony metastases in patients with
carcinoma of the breast. Clinical radiology. 1987;38(4):351-5.
110. Clamp A, Danson S, Nguyen H, Cole D, Clemons M. Assessment of
therapeutic response in patients with metastatic bone disease. The lancet oncology.
2004;5(10):607-16.
111. van den Brekel MW, Castelijns JA, Snow GB. The role of modern imaging
studies in staging and therapy of head and neck neoplasms. Seminars in oncology.
1994;21(3):340-8.
112. Olmi P, Fallai C, Colagrande S, Giannardi G. Staging and follow-up of
nasopharyngeal carcinoma: magnetic resonance imaging versus computerized
tomography. International journal of radiation oncology, biology, physics.
1995;32(3):795-800.
113. Barakos JA, Dillon WP, Chew WM. Orbit, skull base, and pharynx:
contrast-enhanced fat suppression MR imaging. Radiology. 1991;179(1):191-8.
114. King
AD,
Bhatia
KS.
Magnetic
resonance
imaging
staging
of
nasopharyngeal carcinoma in the head and neck. World journal of radiology.

2010;2(5):159-65.
115. Sellers LM. Cancer of the nasopharynx: Its natural history and treatment.
Archives of Otolaryngology. 1961;74(6):714-5.
.
102
References
116. Hyare H, Wisco JJ, Alusi G, Cohen M, Nabili V, Abemayor E, Kirsch CF.
The anatomy of nasopharyngeal carcinoma spread through the pharyngobasilar
fascia to the trigeminal mandibular nerve on 1.5 T MRI. Surgical and radiologic
anatomy. 2010;32(10):937-44.
117. Liu L, Liang S, Li L, Mao Y, Tang L, Tian L, Liao X, Cui C, Lin A, Ma J.
Prognostic impact of magnetic resonance imagingdetected cranial nerve
involvement in nasopharyngeal carcinoma. Cancer. 2009;115(9):1995-2003.
118. Stambuk HE. Perineural tumor spread involving the central skull base
region. Seminars in ultrasound, CT, and MR. 2013;34(5):445-58.
119. Williams LS, Mancuso AA, Mendenhall WM. Perineural spread of
cutaneous squamous and basal cell carcinoma: CT and MR detection and its
impact on patient management and prognosis. International Journal of Radiation
Oncology, Biology, Physics. 2001;49(4):1061-9.
120. Chan M, Bartlett E, Sahgal A, Yu E. Imaging of nasopharyngeal cancer. In:
Carcinogenesis, diagnosis, and molecular targeted treatment for nasopharyngeal
cancer. InTech. Rijeka, Croatia. 2012. 95-122.
121. King AD, Lam W, Leung SF, Chan Y, Teo P, Metreweli C. MRI of local
disease in nasopharyngeal carcinoma: tumour extent vs tumour stage. British
journal of radiology. 1999;72(860):734-41.
122. Caldemeyer KS, Mathews VP, Righi PD, Smith RR. Imaging features and
clinical significance of perineural spread or extension of head and neck tumors.
Radiographics. 1998;18(1):97-110.
103
References
123. Liao X-B, Mao Y-P, Liu L-Z, Tang L-L, Sun Y, Wang Y, Lin AH, Cui
CY, Li L, Ma J. How does magnetic resonance imaging influence staging
according to AJCC staging system for nasopharyngeal carcinoma compared with
computed tomography? International Journal of Radiation Oncology, Biology,
Physics. 2008;72(5):1368-77.
124. Ng SH, Chan SC, Yen TC, Chang JT, Liao CT, Ko SF, Liu FY, Chin
SC, Fan KH, Hsu CL. Staging of untreated nasopharyngeal carcinoma with
PET/CT: comparison with conventional imaging work-up. European journal of
nuclear medicine and molecular imaging. 2009;36(1):12-22.
125. Sakata K, Hareyama M, Tamakawa M, Oouchi A, Sido M, Nagakura
H, Akiba H, Koito K, Himi T, Asakura K. Prognostic factors of nasopharynx
tumors investigated by MR imaging and the value of MR imaging in the newly
published TNM staging. International Journal of Radiation Oncology, Biology,
Physics. 1999;43(2):273-8.
126. Van Den Brekel MW, Castelijns JA, Snow GB. The role of modern imaging
studies in staging and therapy of head and neck neoplasms. Seminars in oncology.
1994;21(3):340-8.
127. Mineura K, Kowada M, Tomura N. Perineural extension of nasopharyngeal
carcinoma into the posterior cranial fossa detected by magnetic resonance imaging.
Clinical imaging. 1991;15(3):172-5.
128. Chong VF, Fan Y-F, Khoo JB. Nasopharyngeal carcinoma with intracranial
spread: CT and MR characteristics. Journal of computer assisted tomography.
1996;20(4):563-9.
104
References
129. Chong VF, Khoo JB, Fan YF. Imaging of the nasopharynx and skull base.
Neuroimaging clinics of North America. 2004;14(4):695-719.
130. Wintermark M, Wirt MD, Mukherjee P, Zaharchuk G, Barbier E, Dillon
WP, Ertl-Wagner BB, Rummeny C, Essig M, Bergen DC, Fagnou JM, Sevick R,
Tali ET, Gltekin S, Karimi S, Holodny AI, Kanagaki M, Sato N, Miki Y, Hosten
N, Zwicker B, Langer M, Maroldi R, Farina D, Borghesi A, Botturi E, Ambrosi C,
Stambuk H, Fischbein N. Brain, Head, and Neck. In: Reiser MF, Semmler W,
Hricak H, editors. Magnetic Resonance Tomography: Springer Berlin Heidelberg;
2008. p. 169-533.
131. Nilssen E, McClymont L, Denholm S. Radiological staging for squamous
carcinoma of the head and neck: a standardised practice? Journal of the Royal
College of Surgeons of Edinburgh. 1999;44(5):303-6.
132. Glastonbury CM. Nasopharyngeal carcinoma: the role of magnetic
resonance imaging in diagnosis, staging, treatment, and follow-up. Top Magn
Reson Imaging. 2007 Aug;18(4):225-35.
133. Gor DM, Langer JE, Loevner LA. Imaging of cervical lymph nodes in head
and neck cancer: the basics. Radiol Clin North Am. 2006;44(1):101-10.
134. Som PM. Lymph nodes of the neck. Radiology. 1987;165(3):593-600.
135. King AD, Tse GM, Ahuja AT, Yuen EH, Vlantis AC, To EW, van Hasselt
AC. Necrosis in metastatic neck nodes: diagnostic accuracy of CT, MR imaging,
and US. Radiology. 2004;230(3):720-6.
136. Chong V, FAN Y-F. Facial lymphadenopathy in nasopharyngeal carcinoma.
Clinical radiology. 2000;55(5):363-7.
105
References
137. Ng SH, Chang JT, Chan SC, Ko SF, Wang HM, Liao CT, Chang YC, Yen
TC. Nodal metastases of nasopharyngeal carcinoma: patterns of disease on MRI
and FDG PET. European journal of nuclear medicine and molecular imaging.
2004;31(8):1073-80.
138. Wang XS, Hu CS, Ying HM, Zhou ZR, Ding JH, Feng Y. Patterns of
retropharyngeal node metastasis in nasopharyngeal carcinoma. International
Journal of Radiation Oncology Biology Physics. 2009;73(1):194-201.
139. King AD, Ahuja AT, Leung Sf, Lam WW, Teo P, Chan Yl, Metreweli C.
Neck node metastases from nasopharyngeal carcinoma: MR imaging of patterns of
disease. Head & neck. 2000;22(3):275-81.
140. Liu L-Z, Zhang G-Y, Xie C-M, Liu X-W, Cui C-Y, Li L. Magnetic
resonance imaging of retropharyngeal lymph node metastasis in nasopharyngeal
carcinoma: patterns of spread. International Journal of Radiation Oncology,
Biology, Physics. 2006;66(3):721-30.
141. Mao YP, Liang SB, Liu LZ, Chen Y, Sun Y, Tang LL, Tian L, Lin AH, Liu
MZ, Li L, Ma J. The N staging system in nasopharyngeal carcinoma with radiation
therapy oncology group guidelines for lymph node levels based on magnetic
resonance imaging. Clinical Cancer Research. 2008;14(22):7497-503.
142. Wang XS, Hu CS, Ying HM, Zhou ZR, Ding JH, Feng Y. Patterns of
retropharyngeal node metastasis in nasopharyngeal carcinoma. International
journal of radiation oncology, biology, physics. 2009;73(1):194-201.
143. Som P, Brandwein M. Lymph nodes. Head and neck imaging. 2003;2:77293.
106
References
144. Yousem DM, Som PM, Hackney DB, Schwaibold F, Hendrix RA. Central
nodal necrosis and extracapsular neoplastic spread in cervical lymph nodes: MR
imaging versus CT. Radiology. 1992;182(3):753-9.
145. Yu E, O'Sullivan B, Kim J, Siu L, Bartlett E. Magnetic resonance imaging of
nasopharyngeal carcinoma. Expert review of anticancer therapy. 2010;10(3):36575.
146. Hillsamer PJ, Schuller DE, McGhee Jr RB, Chakeres D, Young DC.
Improving diagnostic accuracy of cervical metastases with computed tomography
and magnetic resonance imaging. Archives of Otolaryngology-Head & Neck
Surgery. 1990;116(11):1297-301.
147. Crawford SC, Harnsberger HR, Lufkin RB, Hanafee WN. The role of
gadolinium-DTPA in the evaluation of extracranial head and neck mass lesions.
Radiol Clin North Am. 1989;27(2):219-42.
148. Abdel Khalek Abdel Razek A, King A. MRI and CT of nasopharyngeal
carcinoma. AJR Am J Roentgenol. 2012;198(1):11-8.
149. King AD, Ma BB, Yau YY, Zee B, Leung SF, Wong JK, Kam MK, Ahuja
AT, Chan AT. The impact of 18F-FDG PET/CT on assessment of nasopharyngeal
carcinoma at diagnosis. The British journal of radiology. 2008;81(964):291-8.
150. Chang JT, Lin CY, Chen TM, Kang CJ, Ng SH, Chen IH, Wang HM, Cheng
AJ, Liao CT. Nasopharyngeal carcinoma with cranial nerve palsy: the importance
of MRI for radiotherapy. International journal of radiation oncology, biology,
physics. 2005;63(5):1354-60.
107
References
151. Chung NN, Ting LL, Hsu WC, Lui LT, Wang PM. Impact of magnetic
resonance imaging versus CT on nasopharyngeal carcinoma: primary tumor target
delineation for radiotherapy. Head & neck. 2004;26(3):241-6.
108
Protocol

Protocol of a thesis submitted
to the Faculty of Medicine
In partial fulfillment of the
requirements of the degree of
Master of Radiodiagnosis and
Intervention
by
MBBCh, Alex.
Visiting Resident
Alexandria University Hospitals
Department of Radiodiagnosis
Faculty of Medicine
2011
2011
109
Protocol
SUPERVISORS
Prof. Dr. Shadya Abu Seif Helmy

Professor of Radiodiagnosis,
Faculty of Medicine,
University of Alexandria.
Prof. Dr. Mohamed Basiouny Atalla

Professor of Otorhinolaryngology
/..

/..

CO-SUPERVISOR
Ass. Prof. Dr. Mohamed Eid Ibrahim

Assistant professor in Radiodiagnosis
Faculty of Medicine
For his experience in Head and Neck
Imaging by CT and MRI
/ ..

Protocol
CO-RESEARCHER
Ahmed Hammouda Husam Eldin
Fifth grade student
Mobile phone: 0105440517
E-mail: dochamouda@yahoo.com
Protocol
INTRODUCTION
Nasopharyngeal cancer (NPC) is a unique disease that shows clinical
behavior, epidemiology and histopathology that is different from that of other
squamous cell carcinomas of the head and neck. (1)
Nasopharyngeal cancer is a squamous cell carcinoma arising from the
pharyngeal mucosal space of the nasopharynx. Three histolopathological
subtypes of NPC are recognized by World Health organization (WHO),
(2)
which vary in their clinical behavior and prognostic significance: Type I

(keratinizing squamous cell carcinoma) is the least common, carries the least
favorable prognosis, Type II (non-keratinizing squamous cell carcinoma),
and Type III (undifferentiated carcinoma) are more common, carry a more
favorable prognosis and are more sensitive to radiotherapy.
NPC presents most commonly as a unilateral neck lump in 50% to
70% of patients, from cervical lymph node metastases; the tumor may not be
clinically apparent at the time of presentation. (3) Eustachian tube obstruction
may produce persistent unilateral hearing loss or otitis media. Other
presenting features include a bloody nasal discharge or less frequently,
cranial nerve palsies. The peak incidence is usually in the 5 th to 6th decades,
also the peak years of economic productivity for individuals.
Endoscopic evaluation of the nasopharynx with biopsy is performed in
patients suspected of having NPC, particularly if risk factors are present.
However, tumors may be clinically occult. Also, the deep extensions of
visible tumors cannot be assessed by endoscopy and clinical examination.
(4, 5)
Imaging modalities including contrast enhanced computed tomography (CT)

and magnetic resonance imaging (MRI) are mandatory for staging and
evaluation. (6)
1
Protocol
The primary tumor extent should be evaluated by both CT scan and

MRI. The later is more sensitive than CT scan for the detection of the
primary tumor, its direct soft tissue extent, regional nodal metastasis and
perineural extension. Blood vessels are clearly shown by MRI even without
the use of intravenous contrast.
(7)
On the other hand, although MRI can also
demonstrate erosion into the base of the skull by virtue of the change in the
signal of fatty bone marrow, CT scan is generally considered a more sensitive
tool for defining bone erosion. (8 -10)
In this study, staging of the nasopharyngeal carcinoma by CT and MRI
will be described, referring to the latest TNM classification used by the
AJCC. (11)
Protocol
AIM OF THE WORK

The aim of this work is to describe the role of state of the art cross
sectional imaging computed tomography and magnetic resonance imaging
(CT&MRI) in the staging of nasopharyngeal carcinoma.
Protocol
PATIENTS
The study will be conducted on 20 patients referred to the
Radiodiagnosis Department at the Alexandria Main University Hospital
presenting with pathologically proven nasopharyngeal carcinoma.
Protocol
METHODS
Selected patients will be subjected to:
Informed written consent taking.
History taking.
Thorough clinical examination.
Routine laboratory investigations.
Plain and Enhanced Multi-detector Computed Tomography of the

neck.
MRI examination
T1-weighted spin-echo.
Contrastenhanced T1-weighted spin-echo imaging.
T2-weighted spin-echo.
Diffusion weighted images whenever possible.
Endoscopic examination and biopsy from the suspected area with

routine histopathologic examination.
Correlation with pathological data.
Protocol
RESULTS
The results of this study will be calculated, tabulated and statistically
analyzed according to the appropriate methods.
Protocol
DISCUSSION
The results will be discussed in view of achievement of the aim, their
significance and their comparison with previous related researches, in the
literature.
Protocol
REFERENCES
1. Imaging of NPCJulian Goh and Keith Lim, Ann Acad Med Singapore
2009;38:809-16
2. Shanmugaratnam K, Sobin LH. The World Health Organization histological
classification of tumours of the upper respiratory tract and ear. A commentary

on the second edition. Cancer 1993; 71:2689-97
3. Pathmanathan
R.
Pathology.
In:
Chong
VFH,
Tsao
SY,
editors.
Nasopharyngeal Carcinoma. Hong Kong: Armour Publishing, 1997:6-13

4. Wei WI, Sham JS, Zong YS, Choy D, Ng MH. The efficacy of fiberoptic
endoscopic examination and biopsy in the detection of early nasopharyngeal

carcinoma. Cancer 1991; 67 (12): 3127 30
5. Sham JS, Wei WI, Kwan WH, Chan CW, Choi PH, Choy D. Fiberoptic
endoscopic
examination
and
biopsy
in
determining
the
extent
of
nasopharyngeal carcinoma. Cancer 1989; 64 (9): 1838 42

6. Ng SH, Chang TC, Ko SF, et al. Nasopharyngeal carcinoma: MRI and CT
assessment. Neuroradiology 1997; 39:7416

7. King AD, Lam W, Leung SF, et al. MR imaging of local disease in
nasopharyngeal carcinoma: tumor extent vs. tumor stage. BJR 1999; 2:73441
8. Chong VF, Fan YF. Skull base erosion in nasopharyngeal carcinoma: detection
by CT and MRI. Clin Radiol 1996; 51:62531

9. Poon PY, Tsang VH, Munk PL. Tumor extent and T stage of nasopharyngeal
carcinoma: a comparison of magnetic resonance imaging and computed

tomographic findings. Can Assoc Radiol J 2000;51:28795
10. King AD, Teo P, Lam WWM, et al.: Staging of paranasopharyngeal tumor
extension in nasopharyngeal carcinoma: MR vs. CT imaging. Clin Oncol 2000;

12:397402
11. Edge SB, Byrd DR, Compton CC, et al, eds. Pharynx. In: AJCC Cancer Staging
Manual. 7th ed. New York, NY: Springer; 2010:41-9

.

.
20 .

.

.

.

( ).

.
.

.
T1
.

.

.
T1
.

.

.
.

.

. /
.......................................

. /
.......................................

. /
.......................................

---------/---/---:
. /

....................................

. /

....................................

. . /

....................................

Nasopharyngeal Carcinoma Staging by CT and MRI

Încărcat de

Informații document

Drepturi de autor

Formate disponibile

Partajați acest document

Partajați sau inserați document

Opțiuni de partajare

Vi se pare util acest document?

Este necorespunzător acest conținut?

Drepturi de autor:

Formate disponibile

Nasopharyngeal Carcinoma Staging by CT and MRI

Încărcat de

Drepturi de autor:

Formate disponibile

NASOPHARYNGEAL CARCINOMA

STAGING BY COMPUTED TOMOGRAPHY AND

Islam Mohamed El Gezeiry

Islam Mohamed El Gezeiry

Prof. Dr. Shadia Abou Seif Helmy

Prof. Dr. Mahmoud Lotfy El-Sheikh

Prof. Dr. Shadia Abou Seif Helmy

Ass. Prof. Dr. Mohamed Eid Ibrahim

Shadia Abou Seif Helmy, Professor of Radiodiagnosis, Faculty of

Ibrahim, Assistant Professor in Radiodiagnosis, Faculty of Medicine,

AIM OF THE WORK------------------------------

PATIENTS AND METHODS---------------------

Pharyngeal mucosal space

World Health Organization

American Joint Committee on Cancer

Intensity Modulated Radiotherapy

Combined chemotherapy and radiotherapy

Retropharyngeal lymph nodes

Distribution of studied cases according to demographic

Distribution of studied cases according to side involved

Distribution of studied cases according to neck spaces

Distribution of studied cases according to extension

Distribution of studied cases according to paranasal sinus

Distribution of studied cases according to pterygopalatine

Distribution of studied cases according to skull base bone

Distribution of studied cases according to foramina

Distribution of studied cases according to perineural

Distribution of studied cases according to lymph nodal

Distribution of studied cases with cervical

Distribution of studied cases according to primary tumor

Distribution of studied cases according to lymph nodes

Distribution of studied cases according to TNM stage

A graphic of skull base from below shows spaces of

suprahyoid neck relationships to skull base with emphasis on

Axial graphic of the nasopharyngeal mucosal space.

Mid-line sagittal graphic of the nasopharynx.

Lateral radiograph of the nasopharynx showing enlarged

A graphic showing the lateral wall structures of the

Spaces related to the nasopharynx.

margins of the levels of the imaging-based classification for the lymph

A lateral radiograph of mildly enlarged adenoid.

The superior end of the para-pharyngeal space just before it

abuts the skull base.

Axial T2w image at the level of the opening of the Eustachian

Axial T1w image of the pharyngeal mucosal space at the

level of the Eustachian tube opening.

Sagittal T1w image of the pharynx.

Coronal enhanced fat-saturated T1 MR image.

Coronal enhanced fat-saturated T1w MR Image.

the related spaces.

Shaded triangular area corresponding to the supraclavicular

fossa used in staging carcinoma of the nasopharynx.

(Right)Axial T2wI MR shows large right NP mass.

(Left) Axial bone CT showing enlarged right foramen ovale.

Patient presenting with a left nasopharyngeal tumor.

Axial TSE T2-weighted image showing left nasopharyngeal

tumor extending to the pterygo-palatine fossa.

Contrast-enhanced SE T1-weighted MR images with fat

saturation illustrating different pathways of extension in a

Contrast-enhanced T1-weighted MR images in a patient

presenting with direct lateral extension through the

Spread of an advanced nasopharyngeal tumor.

(a) Non-enhanced T1-weighted MR image without fat

saturation of a nasopharyngeal tumor infiltrating the clivus